Details of the Researcher

PHOTO

Shiori Minabe
Section
Tohoku Medical Megabank Organization
Job title
Senior Assistant Professor
Degree
e-Rad No.
40781571

Research History 8

  • 2026/04 - Present
    Tohoku University　Tohoku Medical Megabank Organization Department of Integrative Genomics

  • 2021/07 - 2026/04
    Iwate Medical University　Iwate Tohoku Medical Megabank Organization　project assistant professor

  • 2020/04 - 2021/06
    日本医科大学 大学院医学研究科　解剖学・神経生物学分野　日本学術振興会特別研究員 (RPD)

  • 2018/04 - 2020/03
    Nippon Medical School　Laboratory of Anatomy

  • 2017/04 - 2018/03
    The University of Tokyo　Graduate School of Agricultural and Life Sciences

  • 2016/04 - 2017/03
    The University of Tokyo　Graduate School of Agricultural and Life Sciences

  • 2015/04 - 2016/03
    農業・食品産業技術総合研究機構 畜産草地研究所　契約研究員

  • 2012/04 - 2015/03
    名古屋大学大学院　日本学術振興会特別研究員 (DC1)

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Education 4

  • 名古屋大学大学院　生命農学研究科 (博士後期課程)

    2012/04 - 2015/03

  • 名古屋大学大学院　生命農学研究科 (博士前期課程)

    2010/04 - 2012/03

  • Nagoya University　School of Agricultural Sciences

    2006/04 - 2010/03

  • Meiwa High School

    2003/04 - 2006/03

Professional Memberships 6

  • 日本組織細胞化学会

    2020/08 - Present

  • Endocrine Society

    2018/12 - Present

  • 日本内分泌学会

    2017/10 - Present

  • 日本生殖内分泌学会

    2017/08 - Present

  • 日本神経内分泌学会

    2016/10 - Present

  • SOCIETY FOR REPRODUCTION AND DEVELOPMENT

    2010/06 - Present

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Research Interests 3

  • 生殖神経内分泌

  • ゲノムオミックス

  • バイオインフォマティクス

Research Areas 2

  • Life sciences / Systems genomics /

  • Life sciences / Animals: biochemistry, physiology, behavioral science /

Awards 4

  1. the Eugenia Rosemberg Abstract Travel Award

    2018/03　Endocrine Society

  2. 学術奨励賞

    2017/09　日本生殖内分泌学会

  3. 最優秀発表賞

    2014/08　日本下垂体研究会

  4. 名古屋大学総長賞

    2011/11　若手女性研究者サイエンスフォーラム

Papers 40

  1. Inter-individual differentially methylated region-targeted EWAS reveals epigenetic signatures of early childhood adversity. International-journal

    Taira Mayanagi, Junko Yagi, Hideki Ohmomo, Manami Akasaka, Kentaro Fukumoto, Shusaku Chiba, Shohei Komaki, Atsushi Shimizu, Takehito Yanbe, Mare Uchide, Yasuhito Yoshioka, Kaori Ogawa, Chiho Ishikawa, Shiori Minabe, Jun Ito, Kanako Ono, Nozomi Kaneko, Kenji Sobue

    Epigenomics　1-12　2026/01/07

    DOI： 10.1080/17501911.2026.2613008 　

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    AIMS: Adverse childhood experiences (ACEs), especially in early life, can affect psychosocial development and increase lifelong risk for mental disorders. ACEs are also known to induce persistent epigenetic changes. This study aimed to explore ACE-associated DNA methylation signatures using an epigenome-wide association study (EWAS) targeting inter-individual differentially methylated regions (DMRs). METHODS: We developed a targeted capture probe system covering ~1.3 million CpG sites within inter-individual DMRs. This system was applied to salivary DNA from drug-naïve children aged 6-12 years with exposure to multiple early-life ACEs (n = 23) or who had no ACEs (n = 21). RESULTS: We identified 15 novel DMRs significantly associated with ACEs. A cluster of six CpG sites within an exon of the EIF4G2 gene showed consistently increased methylation in children with ACEs, with strong inter-site correlations. Enrichment analysis indicated that genes near these DMRs are involved in neurodevelopmental disorders, suggesting that early adversity may influence brain development through epigenetic mechanisms. CONCLUSION: Our findings suggest that early adversity may contribute to lasting epigenetic modifications in children. The identified DMRs may serve as noninvasive biomarkers for retrospective ACE assessment and provide insights into the biological embedding of early-life stress.

  2. Study Profile of the Iwate PGS Assessment and Risk Communication (PARC) Study. Peer-reviewed

    Akiko Yoshida, Tomoharu Tokutomi, Nobuhiro Suzumori, Akimune Fukushima, Yukiko Toya, Hideki Ohmomo, Kozo Tanno, Yoichi Sutoh, Yuka Kotozaki, Tsuyoshi Hachiya, Kazuki Kumada, Hisaaki Kudo, Atsushi Hasegawa, Mika Sakurai-Yageta, Akira Narita, Yohei Hamanaka, Satoshi Nagaie, Soichi Ogishima, Fuji Nagami, Yayoi Otsuka-Yamasaki, Shohei Komaki, Shiori Minabe, Koichi Asahi, Ryujin Endo, Yasushi Ishigaki, Masayuki Yamamoto, Atsushi Shimizu, Makoto Sasaki

    Journal of epidemiology　2025/09/06

    DOI： 10.2188/jea.JE20250078 　

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    BACKGROUND: The potential impacts of polygenic scores (PGS) on health-behavior changes are not fully understood. The Iwate PGS Assessment and Risk Communication Study aims to investigate the effects of reporting PGS-based risk for ischemic stroke on health behaviors. METHODS: Participants wishing to know their PGS-based ischemic stroke risk were recruited from health checkup venues for workers in Iwate Prefecture in 2023. Health checkup data, biospecimens, and questionnaire responses were collected for biochemical testing, genotyping, and storage in the Tohoku Medical Megabank integrated biobank. The risk was calculated using an integrative PGS model for East Asians. Participants were randomly assigned to two groups, and one group received their risk report as the intervention group. The impacts of the risk notification will be investigated in follow-up surveys. RESULTS: Of 3,599 workers, 2,088 participated in the study (consent rate, 58.0%). The demographic profile of the eligible 2,083 participants was as follows: 80.7% males, and dominance of participants aged 18-29 years (25.2%), in their 30's (25.3%), and in their 40's (24.7%). Two hundred participants (9.7%) had a risk of 1.0 as the reference; 57 (2.7%), 927 (44.7%), and 888 (42.9%) participants had 2.1-3.4-, 1.4-1.9-, and <1.0-fold that risk, respectively. CONCLUSION: We collected health information and biospecimens from over 2,000 workers, and disclosed the PGS-based ischemic stroke risk. Behavioral effects will be evaluated 1 year after disclosure, with follow-up until 2030. As Japan's first large-scale PGS risk communication study, it will provide initial insights for implementing PGS in personalized preventive medicine.

  3. Exploring novel blood-based DNA methylation biomarkers for alzheimer's disease via targeted sequencing of highly variable CpG sites. International-journal Peer-reviewed

    Hideki Ohmomo, Shohei Komaki, Shiori Minabe, Yoichi Sutoh, Yayoi Otsuka-Yamasaki, Makoto Sasaki, Atsushi Shimizu

    BMC research notes　18　(1)　350-350　2025/08/12

    DOI： 10.1186/s13104-025-07417-7 　

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    OBJECTIVE: Dementia, particularly Alzheimer’s disease (AD), continues to be a major public health concern due to population aging, yet minimally invasive biomarkers for early diagnosis have not been established. DNA methylation (DNAm) has recently attracted considerable attention as a promising biomarker. This study aimed to identify blood-based DNAm biomarkers for early detection of AD. RESULTS: We analysed blood-derived DNA from 48 patients with AD (from Biobank Japan) and 48 age- and sex-matched controls (from the Tohoku Medical Megabank Biobank) using Apolipoprotein ε type 4 (APOE)-associated genotype analysis and targeted-bisulfite sequencing. High-risk APOE genotypes were more frequent in AD patients (23/48, [47.9%]) than in controls (6/48, [12.5%]). A typical case-control and APOE genotype-stratified epigenome-wide association study (EWAS) did not identify any genome-wide significant CpG sites. Although the primary findings were negative, some top CpG sites appeared in both analyses, including loci on the Cell Adhesion Molecule 1 (CADM1), Tubulin alpha 1b (TUBA1B), and Exocyst complex component 2 (EXOC2) genes, which have previously been linked to AD-related pathways. The relatively early clinical stage and uncertainty of disease onset might have limited detection sensitivity. Longitudinal studies with refined staging and multi-omics integration might clarify the biomarker potential of blood DNAm in AD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-025-07417-7.

  4. Genetic predisposition for immunoglobulin E production explains atopic risk in children: Tohoku Medical Megabank cohort study. International-journal Peer-reviewed

    Yoichi Sutoh, Tsuyoshi Hachiya, Yayoi Otsuka-Yamasaki, Shohei Komaki, Shiori Minabe, Hideki Ohmomo, Kozo Tanno, Atsushi Hozawa, Naoki Nakaya, Aoi Noda, Masatsugu Orui, Mami Ishikuro, Taku Obara, Shinichi Kuriyama, Makoto Sasaki, Atsushi Shimizu

    American journal of human genetics　2025/07/15

    DOI： 10.1016/j.ajhg.2025.06.015 　

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    The atopic march lacks early identification methods for high-risk children. In this study, we assessed whether the risk of atopic diseases in infants could be predicted using a polygenic score (PGS) for total immunoglobulin E (IgE) levels. The PGS estimated using the polygenic model generated by PRS-CS was significantly correlated with log-transformed IgE levels (ρ = 0.200, p < 2.2 × 10-16). Assessment of the risk from birth to 2 years of age in a Japanese birth cohort (n = 17,154) applying the estimated PGS revealed significantly elevated incidence risk ratios in the highest PGS quintile (Q5) compared with those in the reference quintiles (Q1-Q3) for food allergy (1.51-fold; 95% confidence interval: 1.30-1.76), atopic dermatitis (1.30-fold; 1.12-1.51), and both conditions (1.88-fold; 1.46-2.43). These findings address critical gaps in allergy and PGS research among non-European populations, suggesting the contribution of genetic predisposition to IgE production in early-onset allergic diseases and supporting the use of PGS in early intervention.

  5. Risk factors and prediction for pediatric obesity: current status and future perspectives.

    Shiori Minabe, Yoichi Sutoh, Yayoi Otsuka-Yamasaki, Shohei Komaki, Motoki Nakao, Hideki Ohmomo, Yutaka Hasegawa, Yasushi Ishigaki, Kozo Tanno, Makoto Sasaki, Atsushi Shimizu

    Endocrine journal　2025/04/09

    DOI： 10.1507/endocrj.EJ24-0724 　

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    Childhood obesity is a growing global health concern, contributing to numerous non-communicable diseases and long-term health complications. The prevalence of obesity in children and adolescents continues to rise, driven by complex interactions among various factors. The key risk factors include both environmental and genetic influences. Environmental factors include family elements like household conditions and lifestyle, while genetic factors refer to inherited predispositions. More recently, epigenetic factors have gained attention, focusing on chemical modifications such as DNA methylation that are influenced by the prenatal and early-life environment and may contribute to obesity risk. Unlike obesity in adults, the risk factors for obesity in children are largely dependent on their family environments rather than individual behaviors. For effective intervention, it is important to identify at-risk children and their families as early as possible after birth. Despite advances in machine learning, polygenic risk scores, and epigenomic markers-which show promise as being more accurate and comprehensive prediction methods-no risk prediction models are currently in clinical use. Achieving predictions with higher accuracy, external validation, and consideration of population-specific factors (e.g., ethnic variability) while avoiding bias or stigma in targeted interventions is needed for effective childhood obesity prevention. Herein, we summarize environmental, genetic, and epigenetic risk factors for childhood obesity and review the unique situations and regional factors in Japan, which are the focus of our study. Furthermore, we introduce the major advances in risk prediction models for childhood obesity.

  6. Reference-Based Standardization Approach Stabilizing Small Batch Risk Prediction via Polygenic Score. International-journal Peer-reviewed

    Yoichi Sutoh, Tsuyoshi Hachiya, Yayoi Otsuka-Yamasaki, Tomoharu Tokutomi, Akiko Yoshida, Yuka Kotozaki, Shohei Komaki, Shiori Minabe, Hideki Ohmomo, Kozo Tanno, Akimune Fukushima, Makoto Sasaki, Atsushi Shimizu

    Genetic epidemiology　49　(2)　e70002　2025/03

    DOI： 10.1002/gepi.70002 　

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    The polygenic score (PGS) holds promise for motivating preventive behavioral changes. However, no clinically validated standardization methodology currently exists. Here, we demonstrate the efficacy of a "reference-based" approach for standardization. This method uses the PGS distribution in the general population as a reference for normalization and percentile determination; however, it has not been validated. We investigated three potential influences on PGS computation: (1) the size of the reference population, (2) biases associated with different genotyping platforms, and (3) inclusion of kinship ties within the reference group. Our results indicate that the reference size affects the bootstrap estimate of standard error for PGS percentiles, peaking around the 50th percentile and diminishing at extreme percentiles (1st or 100th). Discrepancies between genotyping platforms, such as different microarrays and whole-genome sequencing, resulted in deviations in PGS (p < 0.05 in Kolmogorov-Smirnov test). However, these deviations were reduced to a nonsignificant level using shared genetic variants in the calculations when the ancestry of the samples and reference were matched. This approach recovered approximately 9.6% of the positive predictive value of PGS by naïve genotype. Our results provide fundamental insights for establishing clinical guidelines for implementing PGS to communicate reliable risks to individuals.

  7. Healthy lifestyle practice correlates with decreased obesity prevalence in individuals with high polygenic risk: TMM CommCohort study. International-journal Peer-reviewed

    Yoichi Sutoh, Tsuyoshi Hachiya, Yayoi Otsuka-Yamasaki, Shohei Komaki, Shiori Minabe, Hideki Ohmomo, Makoto Sasaki, Atsushi Shimizu

    Journal of human genetics　2024/08/22

    DOI： 10.1038/s10038-024-01280-3 　

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    Obesity and overweight, fundamental components of the metabolic syndrome, predispose individuals to lifestyle-related diseases. The extent to which adopting healthy lifestyles can reduce obesity risk, even in those with a high genetic risk, remains uncertain. Our aim was to assess the extent to which lifestyle modifications can improve outcomes in individuals with a high polygenic score (PGS) for obesity. We quantified the genetic risk of obesity using PGSs. Four datasets from the Tohoku Medical Megabank Community-Based Cohort (TMM CommCohort) were employed in the study. One dataset (n = 9958) was used to select the best model for calculating PGS. The remaining datasets (total n = 69,341) were used in a meta-analysis to validate the model and to evaluate associated risks. The odds ratio (OR) for obesity risk in the intermediate (11th-90th percentiles in the dataset) and high PGS categories (91st-100th) was 2.27 [95% confidence intervals: 2.12-2.44] and 4.83 [4.45-5.25], respectively, compared to that in the low PGS category (1st-10th). Trend analysis showed that an increase in leisure-time physical activity was significantly associated with reduced obesity risk across all genetic risk categories, representing an OR of 0.9 [0.87-0.94] even among individuals in the high PGS category. Similarly, sodium intake displayed a positive association with obesity across all genetic risk categories, yielding an OR of 1.24 [1.17-1.31] in the high PGS category. The risk of obesity was linked to the adoption of healthy lifestyles, even in individuals with high PGS. Our results may provide perspectives for integrating PGSs into preventive medicine.

  8. Central injection of neuropeptide B induces luteinizing hormone release in male and female rats Peer-reviewed

    Youki Watanabe, Kinuyo Iwata, Shiori Minabe, Nobuhiro Nakao, Hirotaka Ishi, Hitoshi Ozawa

    Peptides　171064-171064　2023/07

    Publisher: Elsevier BV

    DOI： 10.1016/j.peptides.2023.171064 　

    ISSN： 0196-9781

  9. Single neonatal estrogen implant sterilizes female animals by decreasing hypothalamic KISS1 expression. International-journal Peer-reviewed

    Chan Jin Park, Shiori Minabe, Rex A Hess, Po-Ching Patrick Lin, Sherry Zhou, Shah Tauseef Bashir, Radwa Barakat, Arnon Gal, CheMyong Jay Ko

    Scientific reports　13　(1)　9627-9627　2023/06/14

    DOI： 10.1038/s41598-023-36727-8 　

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    Reproductive sterilization by surgical gonadectomy is strongly advocated to help manage animal populations, especially domesticated pets, and to prevent reproductive behaviors and diseases. This study explored the use of a single-injection method to induce sterility in female animals as an alternative to surgical ovariohysterectomy. The idea was based on our recent finding that repetitive daily injection of estrogen into neonatal rats disrupted hypothalamic expression of Kisspeptin (KISS1), the neuropeptide that triggers and regulates pulsatile secretion of GnRH. Neonatal female rats were dosed with estradiol benzoate (EB) either by daily injections for 11 days or by subcutaneous implantation of an EB-containing silicone capsule designed to release EB over 2-3 weeks. Rats treated by either method did not exhibit estrous cyclicity, were anovulatory, and became infertile. The EB-treated rats had fewer hypothalamic Kisspeptin neurons, but the GnRH-LH axis remained responsive to Kisspeptin stimulation. Because it would be desirable to use a biodegradable carrier that is also easier to handle, an injectable EB carrier was developed from PLGA microspheres to provide pharmacokinetics comparable to the EB-containing silicone capsule. A single neonatal injection of EB-microspheres at an equivalent dosage resulted in sterility in the female rat. In neonatal female Beagle dogs, implantation of an EB-containing silicone capsule also reduced ovarian follicle development and significantly inhibited KISS1 expression in the hypothalamus. None of the treatments produced any concerning health effects, other than infertility. Therefore, further development of this technology for sterilization in domestic female animals, such as dogs and cats is worthy of investigation.

  10. Effect of a neurokinin 3 receptor-selective agonist administration on the embryos recovered from superovulated cows. International-journal Peer-reviewed

    Shuichi Matsuyama, Sho Nakamura, Shiori Minabe, Satoshi Ohkura, Koji Kimura

    Biology of reproduction　2023/04/19

    DOI： 10.1093/biolre/ioad039 　

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    Superovulation (SOV) treatment of cows results in unovulated follicles and inconsistent quality of the recovered embryos. It has been demonstrated that luteinizing hormone (LH) secretion is suppressed during SOV treatment of cows, which may cause insufficient follicle development and variation in the development of recovered embryos and unovulated follicles. Pulsatile gonadotropin-releasing hormone/LH secretion is controlled by the activity of kisspeptin, neurokinin B, and dynorphin (KNDy) neurons in the arcuate nucleus in many mammals. Since neurokinin B promotes the activity of KNDy neurons, we hypothesized that senktide, a neurokinin B receptor agonist, has potential as a therapeutic drug to improve the ovulation rate and quality of recovered embryos in SOV-treated cows via stimulation of LH secretion. Senktide was administered intravenously (30 or 300 nmol/min) for 2 h, beginning from 72 h after the start of SOV treatment. LH secretion was examined before and after administration, and embryos were collected 7 d after estrus. Senktide administration increased LH secretion in SOV-treated cows. The ratios of code 1, code 1 and 2, and blastocyst stage embryos to recovered embryos were increased by senktide (300 nmol/min) administration. Moreover, the mRNA levels of MTCO1, COX7C, and MTATP6 were upregulated in recovered embryos of senktide (300 nmol/min)-administered animals. These results indicate that the administration of senktide to SOV-treated cows enhances LH secretion and upregulates the expression of genes involved in mitochondrial metabolism in embryos, thereby improving embryo development and embryo quality.

  11. Deterioration of mitochondrial biogenesis and degradation in the endometrium is a cause of subfertility in cows. International-journal Peer-reviewed

    Shuichi Matsuyama, Sho Nakamura, Shiori Minabe, Miki Sakatani, Naoki Takenouchi, Takuya Sasaki, Yuki Inoue, Hisataka Iwata, Koji Kimura

    Molecular reproduction and development　2023/01/16

    DOI： 10.1002/mrd.23670 　

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    To investigate possible causes of reproductive failure, we conducted global endometrial gene expression analyses in fertile and subfertile cows. Ingenuity pathway analysis showed that RICTOR and SIRT3 are significant upstream regulators for highly expressed genes in fertile cows, and are predicted to be activated upstream regulators of normal mitochondrial respiration. Canonical pathway analysis revealed that these highly expressed genes are involved in the activation of mitochondrial oxidative phosphorylation. Therefore, in subfertile cows, the inactivation of RICTOR and SIRT3 may correlate with decreased capacity of mitochondrial respiration. Furthermore, the expression levels of most mitochondrial DNA genes and nuclear genes encoding mitochondrial proteins were higher in subfertile cows. The mitochondrial DNA copy number was significantly higher in the endometrium of subfertile cows, whereas the ATP content did not differ between fertile and subfertile cows. Quantitative reverse transcription-PCR analysis demonstrated that the expression of PGC1a, TFAM, MFN1, FIS1, and BCL2L13 were significantly lower in subfertile cows. In addition, transmission electron microscopy images showed mitochondrial swelling in the endometrial cells of the subfertile cow. These results suggest that poor-quality mitochondria accumulate in the endometrium owing to a reduced capacity for mitochondrial biogenesis, fusion, fission, and degradation in subfertile cows, and may contribute to infertility.

  12. Long-term effects of prenatal undernutrition on female rat hypothalamic KNDy neurons. International-journal Peer-reviewed

    Shiori Minabe, Kinuyo Iwata, Youki Watanabe, Hirotaka Ishii, Hitoshi Ozawa

    Endocrine connections　2022/11/01

    DOI： 10.1530/EC-22-0307 　

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    The nutritional environment during development periods induces metabolic programming, leading to metabolic disorders and detrimental influences on human reproductive health. This study aimed to determine the long-term adverse effect of intrauterine malnutrition on the reproductive center kisspeptin-neurokinin B-dynorphin A (KNDy) neurons in the hypothalamic arcuate nucleus (ARC) of female offspring. Twelve pregnant rats were divided into ad-lib-fed (control, n = 6) and 50% undernutrition (UN, n = 6) groups. The UN group was restricted to 50% daily food intake of the control dams from gestation day 9 until term delivery. Differences between the two groups in terms of various maternal parameters, including body weight (BW), pregnancy duration, and litter size, as well as birth weight, puberty onset, estrous cyclicity, pulsatile luteinizing hormone (LH) secretion, and hypothalamic gene expression of offspring, were determined. Female offspring of UN dams exhibited low BW from birth to 3 weeks, whereas UN offspring showed signs of precocious puberty; hypothalamic Tac3 (a neurokinin B gene) expression was increased in prepubertal UN offspring, and the BW at the virginal opening was lower in UN offspring than that in the control group. Interestingly, the UN offspring showed significant decreases in the number of KNDy gene-expressing cells after 29 weeks of age, but the number of ARC kisspeptin-immunoreactive cells, pulsatile LH secretions, and estrous cyclicity were comparable between the groups. In conclusion, intrauterine undernutrition induced various changes in KNDy gene expression depending on the life stage. Thus, intrauterine undernutrition affected hypothalamic developmental programming in female rats.

  13. Evaluation of short-term epigenetic age fluctuation. International-journal Peer-reviewed

    Shohei Komaki, Hideki Ohmomo, Tsuyoshi Hachiya, Yoichi Sutoh, Kanako Ono, Ryohei Furukawa, So Umekage, Yayoi Otsuka-Yamasaki, Shiori Minabe, Akira Takashima, Kozo Tanno, Makoto Sasaki, Atsushi Shimizu

    Clinical epigenetics　14　(1)　76-76　2022/06/09

    DOI： 10.1186/s13148-022-01293-9 　

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    Considerable effort has been spent on lowering and maintaining the epigenetic age. However, the extent to which epigenetic age fluctuates under normal conditions is poorly understood. Therefore, we analyzed methylation data from monocytes and peripheral blood mononuclear cells collected from two Japanese men. The ranges of the Pan-tissue, Skin and blood, and DNAm PhenoAge epigenetic age during 3 months were ≥ 5.62, ≥ 3.04, and ≥ 8.23 years, and the maximum daily changes were 5.21, 3.20, and 6.53 years, respectively. These fluctuations were not suppressed by correcting for cell-type composition. Although the underlying biological mechanism remains unclear, there was a nonnegligible degree of age fluctuation which should inform personalized clinical applications.

  14. Kiss1-dependent and independent release of luteinizing hormone and testosterone in perinatal male rats. Peer-reviewed

    Jing Chen, Shiori Minabe, Arisa Munetomo, Fumie Magata, Marimo Sato, Sho Nakamura, Masumi Hirabayashi, Yasuhiro Ishihara, Takeshi Yamazaki, Yoshihisa Uenoyama, Hiroko Tsukamura, Fuko Matsuda

    Endocrine journal　69　(7)　797-807　2022/02/05

    DOI： 10.1507/endocrj.EJ21-0620 　

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    Prenatal and postnatal biphasic increases in plasma testosterone levels derived from perinatal testes are considered critical for defeminizing/masculinizing the brain mechanism that regulates sexual behavior in male rats. Hypothalamic kisspeptin neurons are indispensable for stimulating GnRH and downstream gonadotropin, as well as the consequent testicular testosterone production/release in adult male rats. However, it is unclear whether kisspeptin is responsible for the increase in plasma testosterone levels in perinatal male rats. The present study aimed to investigate the role of Kiss1/kisspeptin in generating perinatal plasma LH and the consequent testosterone increase in male rats by comparing the plasma testosterone and LH profiles of wild-type (Kiss1+/+) and Kiss1 knockout (Kiss1-/-) male rats. A biphasic pattern of plasma testosterone levels, with peaks in the prenatal and postnatal periods, was found in both Kiss1+/+ and Kiss1-/- male rats. Postnatal plasma testosterone and LH levels were significantly lower in Kiss1-/- male rats than in Kiss1+/+ male rats, whereas the levels in the prenatal embryonic period were comparable between the genotypes. Exogenous kisspeptin challenge significantly increased plasma testosterone and LH levels and the number of c-Fos-immunoreactive GnRH neurons in neonatal Kiss1-/- and Kiss1+/+ male rats. Kiss1 and Gpr54 (kisspeptin receptor gene) were found in the testes of neonatal rats, but kisspeptin treatment failed to stimulate testosterone release in the cultured testes of both genotypes. These findings suggest that postnatal, but not prenatal, testosterone increase in male rats is mainly induced by central kisspeptin-dependent stimulation of GnRH and consequent LH release.

  15. Morphological Analysis of the Hindbrain Glucose Sensor-Hypothalamic Neural Pathway Activated by Hindbrain Glucoprivation. International-journal Peer-reviewed

    Marimo Sato, Shiori Minabe, Takahiro Sakono, Fumie Magata, Sho Nakamura, Youki Watanabe, Naoko Inoue, Yoshihisa Uenoyama, Hiroko Tsukamura, Fuko Matsuda

    Endocrinology　162　(9)　2021/09/01

    DOI： 10.1210/endocr/bqab125 　

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    Lowered glucose availability, sensed by the hindbrain, has been suggested to enhance gluconeogenesis and food intake as well as suppress reproductive function. In fact, our previous histological and in vitro studies suggest that hindbrain ependymal cells function as a glucose sensor. The present study aimed to clarify the hindbrain glucose sensor-hypothalamic neural pathway activated in response to hindbrain glucoprivation to mediate counterregulatory physiological responses. Administration of 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, into the fourth ventricle (4V) of male rats for 0.5 hour induced messenger RNA (mRNA) expression of c-fos, a marker for cellular activation, in ependymal cells in the 4V, but not in the lateral ventricle, the third ventricle or the central canal without a significant change in blood glucose and testosterone levels. Administration of 2DG into the 4V for 1 hour significantly increased blood glucose levels, food intake, and decreased blood testosterone levels. Simultaneously, the expression of c-Fos protein was detected in the 4V ependymal cells; dopamine β-hydroxylase-immunoreactive cells in the C1, C2, and A6 regions; neuropeptide Y (NPY) mRNA-positive cells in the C2; corticotropin-releasing hormone (CRH) mRNA-positive cells in the hypothalamic paraventricular nucleus (PVN); and NPY mRNA-positive cells in the arcuate nucleus (ARC). Taken together, these results suggest that lowered glucose availability, sensed by 4V ependymal cells, activates hindbrain catecholaminergic and/or NPY neurons followed by CRH neurons in the PVN and NPY neurons in the ARC, thereby leading to counterregulatory responses, such as an enhancement of gluconeogenesis, increased food intake, and suppression of sex steroid secretion.

  16. Testosterone regulation on quiescin sulfhydryl oxidase 2 synthesis in the epididymis. International-journal Peer-reviewed

    Tse-En Wang, Shiori Minabe, Fuko Matsuda, Sheng-Hsiang Li, Hiroko Tsukamura, Kei-Ichiro Maeda, Lee Smith, Laura O'Hara, Bart M Gadella, Pei-Shiue Tsai

    Reproduction (Cambridge, England)　161　(5)　593-602　2021/04/20

    DOI： 10.1530/REP-20-0629 　

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    The epididymis is an androgen-responsive organ, whose structure and functions are modulated by the coordination between androgen and epididymal cues. Highly regulated molecular interaction within the epididymis is required to support viable sperm development necessary for subsequent fertilization. In the present study, we extended our earlier findings on a promising epididymal protein, quiescin sulfhydryl oxidase 2 (QSOX2), and demonstrated a positive correlation between testosterone and QSOX2 protein synthesis through the use of loss- and restore-of-function animal models. Moreover, based on transcriptomic analyses and 2D culture system, we determined that an additional polarized effect of glutamate is indispensable for the regulatory action of testosterone on QSOX2 synthesis. In conclusion, we propose noncanonical testosterone signaling supports epididymal QSOX2 protein synthesis, providing a novel perspective on the regulation of sperm maturation within the epididymis.

  17. Gene-expression profile and postpartum transition of bovine endometrial side population cells†. International-journal Peer-reviewed

    Ryoki Tatebayashi, Sho Nakamura, Shiori Minabe, Tadashi Furusawa, Ryoya Abe, Miki Kajisa, Yasuhiro Morita, Satoshi Ohkura, Koji Kimura, Shuichi Matsuyama

    Biology of reproduction　104　(4)　850-860　2021/04/01

    DOI： 10.1093/biolre/ioab004 　

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    The mechanism of bovine endometrial regeneration after parturition remains unclear. Here, we hypothesized that bovine endometrial stem/progenitor cells participate in the postpartum regeneration of the endometrium. Flow cytometry analysis identified the presence of side population (SP) cells among endometrial stromal cells. Endometrial SP cells were shown to differentiate into osteoblasts and adipocytes. RNA-seq data showed that the gene expression pattern was different between bovine endometrial SP cells and main population cells. Gene Set Enrichment Analysis identified the enrichment of stemness genes in SP cells. Significantly (false discovery rate < 0.01) upregulated genes in SP cells contained several stem cell marker genes. Gene ontology (GO) analysis of the upregulated genes in SP cells showed enrichment of terms related to RNA metabolic process and transcription. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of upregulated genes in SP cells revealed enrichment of signaling pathways associated with maintenance and differentiation of stem/progenitor cells. The terms involved in TCA cycles were enriched in GO and KEGG pathway analysis of downregulated genes in SP cells. These results support the assumption that bovine endometrial SP cells exhibit characteristics of somatic stem/progenitor cells. The ratio of SP cells to endometrial cells was lowest on days 9-11 after parturition, which gradually increased thereafter. SP cells were shown to differentiate into epithelial cells. Collectively, these results suggest that bovine endometrial SP cells were temporarily reduced immediately after calving possibly due to their differentiation to provide new endometrial cells.

  18. Effect of diet-induced obesity on kisspeptin-neurokinin B-dynorphin A neurons in the arcuate nucleus and luteinizing hormone secretion in sex hormone-primed male and female rats. International-journal Peer-reviewed

    Shiori Minabe, Kinuyo Iwata, Hitomi Tsuchida, Hiroko Tsukamura, Hitoshi Ozawa

    Peptides　142　170546-170546　2021/03/29

    DOI： 10.1016/j.peptides.2021.170546 　

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    Metabolic stress resulting from either lack or excess of nutrients often causes infertility in both sexes. Kisspeptin-neurokinin B-dynorphin A (KNDy) neurons in the arcuate nucleus (ARC) has been suggested to be a key players in reproduction via direct stimulation of the pulsatile gonadotropin-releasing hormone (GnRH) and subsequent gonadotropin release in mammalian species. In this study, we investigated the effect of high-fat diet (HFD) on hypothalamic KNDy gene expression to examine the pathogenic mechanism underlying obesity-induced infertility in male and female rats. Male and female rats at 7 weeks of age were fed with either a standard or HFD for 4 months. In the male rats, the HFD caused a significant suppression of ARC Kiss1 and Pdyn gene expressions, but did not affect the plasma luteinizing hormone (LH) levels and sizes of the morphology of the testis and epididymis. In the female rats, 58% of the HFD-fed female rats exhibited irregular estrous cycles, whereas the remaining rats showed regular cycles. Two of the 10 rats that showed HFD-induced irregular estrous cycles showed profound suppression of LH pulse frequency and the number of ARC Kiss1-expressing cells, whereas the other females showed normal LH pulses and ARC Kiss1 expression. Our finding shows that suppression of ARC Kiss1 expression might be the initial pathological change of hypogonadotropic hypogonadism in HFD-fed male rats, while the obese-related infertility in the female rats may be mainly induced by KNDy-independent pathways. Taken together, ARC kisspeptin neurons in male rats may be susceptible to HFD-induced obesity compared with those in female rats.

  19. Inducible Kiss1 knockdown in the hypothalamic arcuate nucleus suppressed pulsatile secretion of luteinizing hormone in male mice. Peer-reviewed

    Shiori Minabe, Sho Nakamura, Eri Fukushima, Marimo Sato, Kana Ikegami, Teppei Goto, Makoto Sanbo, Masumi Hirabayashi, Junko Tomikawa, Takuya Imamura, Naoko Inoue, Yoshihisa Uenoyama, Hiroko Tsukamura, Kei-Ichiro Maeda, Fuko Matsuda

    The Journal of reproduction and development　66　(4)　369-375　2020/08/20

    DOI： 10.1262/jrd.2019-164 　

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    Accumulating evidence suggests that kisspeptin-GPR54 signaling is indispensable for gonadotropin-releasing hormone (GnRH)/gonadotropin secretion and consequent reproductive functions in mammals. Conventional Kiss1 knockout (KO) mice and rats are reported to be infertile. To date, however, no study has investigated the effect of inducible central Kiss1 KO/knockdown on pulsatile gonadotropin release in male mammals. Here we report an in vivo analysis of inducible conditional Kiss1 knockdown male mice. The mice were generated by a bilateral injections of either adeno-associated virus (AAV) vectors driving Cre recombinase (AAV-Cre) or AAV vectors driving GFP (AAV-GFP, control) into the hypothalamic arcuate nucleus (ARC) of Kiss1-floxed male mice, in which exon 3 of the Kiss1 gene were floxed with loxP sites. Four weeks after the AAV-Cre injection, the mice showed a profound decrease in the both number of ARC Kiss1-expressing cells and the luteinizing hormone (LH) pulse frequency. Interestingly, pulsatile LH secretion was apparent 8 weeks after the AAV-Cre injection despite the suppression of ARC Kiss1 expression. The control Kiss1-floxed mice infected with AAV-GFP showed apparent LH pulses and Kiss1 expression in the ARC at both 4 and 8 weeks after the AAV-GFP injection. These results with an inducible conditional Kiss1 knockdown in the ARC of male mice suggest that ARC kisspeptin neurons are responsible for pulsatile LH secretion in male mice, and indicate the possibility of a compensatory mechanism that restores GnRH/LH pulse generation.

  20. GnRH(1-5), a metabolite of gonadotropin-releasing hormone, enhances luteinizing hormone release via activation of kisspeptin neurons in female rats. Peer-reviewed

    Nahoko Ieda, Assadullah, Shiori Minabe, Kana Ikegami, Youki Watanabe, Yusuke Sugimoto, Arisa Sugimoto, Narumi Kawai, Hirotaka Ishii, Naoko Inoue, Yoshihisa Uenoyama, Hiroko Tsukamura

    Endocrine journal　67　(4)　409-418　2020/04/28

    DOI： 10.1507/endocrj.EJ19-0444 　

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    Accumulating evidence suggests that kisspeptin neurons in the arcuate nucleus (ARC), which coexpress neurokinin B and dynorphin, are involved in gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) pulse generation, while the anteroventral periventricular nucleus (AVPV) kisspeptin neurons are responsible for GnRH/LH surge generation. The present study aims to examine whether GnRH(1-5), a GnRH metabolite, regulates LH release via kisspeptin neurons. GnRH(1-5) was intracerebroventricularly injected to ovariectomized and estrogen-treated Wistar-Imamichi female rats. Immediately after the central GnRH(1-5) administration at 2 nmol, plasma LH concentration increased, resulting in significantly higher levels of the area under the curve and baseline of plasma LH concentrations compared to vehicle-injected controls. On the other hand, in Kiss1 knockout rats, GnRH(1-5) administration failed to affect LH secretion, suggesting that the facilitatory effect of GnRH(1-5) on LH release is mediated by kisspeptin neurons. Double in situ hybridization (ISH) for Kiss1 and Gpr101, a GnRH(1-5) receptor gene, revealed that few Kiss1-expressing cells coexpress Gpr101 in both ARC and AVPV. On the other hand, double ISH for Gpr101 and Slc17a6, a glutamatergic marker gene, revealed that 29.2% of ARC Gpr101-expressing cells coexpress Slc17a6. Further, most of the AVPV and ARC Kiss1-expressing cells coexpress Grin1, a gene encoding a subunit of NMDA receptor. Taken together, these results suggest that the GnRH(1-5)-GPR101 signaling facilitates LH release via indirect activation of kisspeptin neurons and that glutamatergic neurons may mediate the signaling. This provides a new aspect of kisspeptin- and GnRH-neuronal communication with the presence of stimulation from GnRH to kisspeptin neurons in female rats.

  21. Colocalization of GPR120 and anterior pituitary hormone-producing cells in female Japanese Black cattle Peer-reviewed

    Sho NAKAMURA, Kohei NODA, Masafumi MIWA, Shiori MINABE, Teruki HAGIWARA, Akira HIRASAWA, Shuichi MATSUYAMA, Ryutaro MORIYAMA

    Journal of Reproduction and Development　66　(2)　135-141　2020

    Publisher: Japanese Society of Animal Reproduction

    DOI： 10.1262/jrd.2019-111 　

    ISSN： 0916-8818

    eISSN： 1348-4400

  22. Neonatal Estrogen Causes Irreversible Male Infertility via Specific Suppressive Action on Hypothalamic Kiss1 Neurons. International-journal Peer-reviewed

    Shiori Minabe, Marimo Sato, Naoko Inoue, Youki Watanabe, Fumie Magata, Fuko Matsuda, Yoshihisa Uenoyama, Hitoshi Ozawa, Hiroko Tsukamura

    Endocrinology　160　(5)　1223-1233　2019/05/01

    DOI： 10.1210/en.2018-00732 　

    ISSN： 0013-7227

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    Aberrant exposure to estrogen-like compounds during the critical developmental period may cause improper hypothalamic programming, thus resulting in reproductive dysfunction in adulthood in male mammals. Kisspeptin-neurokinin B-dynorphin A (KNDy) neurons in the arcuate nucleus (ARC) have been suggested to govern tonic GnRH/gonadotropin release to control reproduction in male mammals. In this study, we report that chronic exposure to supraphysiological levels of estrogen during the neonatal period caused an irreversible suppression of KNDy genes in the ARC, resulting in reproductive dysfunction in male rats. Daily estradiol benzoate (EB) administration from days 0 to 10 postpartum caused smaller seminiferous tubules, abnormal spermatogenesis, and a decrease in plasma testosterone in adult male rats. The neonatal EB treatment profoundly suppressed LH pulse and ARC KNDy gene expression at adulthood, but it failed to affect the number of GnRH gene-expressing cells in male rats. The EB treatment failed to affect gene expression of other neuropeptides, such as GHRH, proopiomelanocortin, and agouti-related protein in the ARC, suggesting that ARC KNDy neurons would be a specific target of neonatal estrogen to cause male reproductive dysfunction. Because LH secretory responses to kisspeptin challenge and GnRH expression were spared in male rats with the EB treatment, LH pulse suppression is most probably due to ARC KNDy deficiency. Taken together, the current study indicates that chronic exposure to estrogenic chemicals in the developing brain causes a defect of ARC KNDy neurons, resulting in an inhibition of pulsatile GnRH/LH release and the failure of spermatogenesis and steroidogenesis.

  23. Morphological analysis for neuronal pathway from the hindbrain ependymocytes to the hypothalamic kisspeptin neurons. Peer-reviewed

    Deura C, Minabe S, Ikegami K, Inoue N, Uenoyama Y, Maeda KI, Tsukamura H

    The Journal of reproduction and development　65　(2)　129-137　2019/04

    DOI： 10.1262/jrd.2018-122 　

    ISSN： 0916-8818

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    Hindbrain ependymocytes are postulated to have a glucose-sensing role in regulating gonadal functions. Previous studies have suggested that malnutrition-induced suppression of gonadotropin secretion is mediated by noradrenergic inputs from the A2 region in the solitary tract nucleus to the paraventricular nucleus (PVN), and by corticotropin-releasing hormone (CRH) release in the hypothalamus. However, no morphological evidence to indicate the neural pathway from the hindbrain ependymocytes to hypothalamic kisspeptin neurons, a center for reproductive function in mammals, currently exists. The present study aimed to examine the existence of a neuronal pathway from the hindbrain ependymocytes to kisspeptin neurons in the arcuate nucleus (ARC) and anteroventral periventricular nucleus (AVPV). To determine this, wheat-germ agglutinin (WGA), a trans-synaptic tracer, was injected into the fourth ventricle (4V) in heterozygous Kiss1-tandem dimer Tomato (tdTomato) rats, where kisspeptin neurons were visualized by tdTomato fluorescence. 48 h after the WGA injection, brain sections were taken from the forebrain, midbrain and hindbrain and subjected to double immunohistochemistry for WGA and dopamine β-hydroxylase (DBH) or CRH. WGA immunoreactivities were found in vimentin-immunopositive ependymocytes of the 4V and the central canal (CC), but not in the third ventricle. The WGA immunoreactivities were detected in some tdTomato-expressing cells in the ARC and AVPV, DBH-immunopositive cells in the A1-A7 noradrenergic nuclei, and CRH-immunopositive cells in the PVN. These results suggest that the hindbrain ependymocytes have neuronal connections with the kisspeptin neurons, most probably via hindbrain noradrenergic and CRH neurons to relay low energetic signals for regulation of reproduction.

  24. Mouse quiescin sulfhydryl oxidases exhibit distinct epididymal luminal distribution with Segment-Specific sperm surface associations. Peer-reviewed

    Wang TE, Li SH, Minabe S, Anderson AL, Dun MD, Maeda KI, Matsuda F, Chang HW, Nixon B, Tsai PJ

    Biology of reproduction　2018/05

    DOI： 10.1093/biolre/ioy125 　

    ISSN： 0006-3363

  25. Correction of a Disease Mutation using CRISPR/Cas9-assisted Genome Editing in Japanese Black Cattle Peer-reviewed

    Mitsumi Ikeda, Shuichi Matsuyama, Satoshi Akagi, Katsuhiro Ohkoshi, Sho Nakamura, Shiori Minabe, Koji Kimura, Misa Hosoe

    SCIENTIFIC REPORTS　7　(1)　17827　2017/12

    DOI： 10.1038/s41598-017-17968-w 　

    ISSN： 2045-2322

  26. Long-Term Neonatal Estrogen Exposure Causes Irreversible Inhibition of LH Pulses by Suppressing Arcuate Kisspeptin Expression via Estrogen Receptors alpha and beta in Female Rodents Peer-reviewed

    Shiori Minabe, Nahoko Ieda, Youki Watanabe, Naoko Inoue, Yoshihisa Uenoyama, Kei-ichiro Maeda, Hiroko Tsukamura

    ENDOCRINOLOGY　158　(9)　2918-2929　2017/09

    DOI： 10.1210/en.2016-1144 　

    ISSN： 0013-7227

    eISSN： 1945-7170

  27. Evidence of involvement of neurone-glia/neurone-neurone communications via gap junctions in synchronised activity of KNDy neurones Peer-reviewed

    K. Ikegami, S. Minabe, N. Ieda, T. Goto, A. Sugimoto, S. Nakamura, N. Inoue, S. Oishi, A. D. Maturana, M. Sanbo, M. Hirabayashi, K. I. Maeda, H. Tsukamura, Y. Uenoyama

    Journal of Neuroendocrinology　29　(6)　12480.　2017/06/01

    DOI： 10.1111/jne.12480 　

    ISSN： 1365-2826 0953-8194

    eISSN： 1365-2826

  28. Molecular and Epigenetic Mechanism Regulating Hypothalamic Kiss1 Gene Expression in Mammals Peer-reviewed

    Yoshihisa Uenoyama, Junk Tomikawa, Naoko Inoue, Teppei Goto, Shiori Minabe, Nahoko Ieda, Sho Nakamura, Youki Watanabe, Kana Ikegami, Fuko Matsuda, Satoshi Ohkura, Kei-ichiro Maeda, Hiroko Tsukamura

    NEUROENDOCRINOLOGY　103　(6)　640-649　2016

    DOI： 10.1159/000445207 　

    ISSN： 0028-3835

    eISSN： 1423-0194

  29. In vitro generation of rabbit anti-Listeria monocytogenes monoclonal antibody using single cell based RT-PCR linked cell-free expression systems Peer-reviewed

    Teruyo Ojima-Kato, Dai Hashimura, Takaaki Kojima, Shiori Minabe, Hideo Nakano

    JOURNAL OF IMMUNOLOGICAL METHODS　427　58-65　2015/12

    DOI： 10.1016/j.jim.2015.10.001 　

    ISSN： 0022-1759

    eISSN： 1872-7905

  30. Pharmacological and Morphological Evidence of AMPK-Mediated Energy Sensing in the Lower Brain Stem Ependymocytes to Control Reproduction in Female Rodents Peer-reviewed

    Shiori Minabe, Chikaya Deura, Kana Ikegami, Teppei Goto, Makoto Sanbo, Masumi Hirabayashi, Naoko Inoue, Yoshihisa Uenoyama, Kei-ichiro Maeda, Hiroko Tsukamura

    Endocrinology　156　(6)　2278-2287　2015/06

    DOI： 10.1210/en.2014-2018 　

    ISSN： 0013-7227

    eISSN： 1945-7170

  31. Lack of pulse and surge modes and glutamatergic stimulation of luteinising hormone release in Kiss1 knockout rats Peer-reviewed

    Y. Uenoyama, S. Nakamura, Y. Hayakawa, K. Ikegami, Y. Watanabe, C. Deura, S. Minabe, J. Tomikawa, T. Goto, N. Ieda, N. Inoue, M. Sanbo, C. Tamura, M. Hirabayashi, K. I. Maeda, H. Tsukamura

    Journal of Neuroendocrinology　27　(3)　187-197　2015/03/01

    DOI： 10.1111/jne.12257 　

    ISSN： 1365-2826 0953-8194

    eISSN： 1365-2826

  32. Identification of Hypothalamic Arcuate Nucleus-Specific Enhancer Region of Kiss1 Gene in Mice Peer-reviewed

    Teppei Goto, Junko Tomikawa, Kana Ikegami, Shiori Minabe, Hitomi Abe, Tatsuya Fukanuma, Takuya Imamura, Kenji Takase, Makoto Sanbo, Koichi Tomita, Masumi Hirabayashi, Kei-ichiro Maeda, Hiroko Tsukamura, Yoshihisa Uenoyama

    MOLECULAR ENDOCRINOLOGY　29　(1)　121-129　2015/01

    DOI： 10.1210/me.2014-1289 　

    ISSN： 0888-8809

  33. KISS1 Gene Expression in the Developing Brain of Female Pigs in Pre- and Peripubertal Periods Peer-reviewed

    Nahoko Ieda, Yoshihisa Uenoyama, Yoko Tajima, Tomoko Nakata, Masatoshi Kano, Yousuke Naniwa, Youki Watanabe, Shiori Minabe, Junko Tomikawa, Naoko Inoue, Fuko Matsuda, Satoshi Ohkura, Kei-ichiro Maeda, Hiroko Tsukamura

    JOURNAL OF REPRODUCTION AND DEVELOPMENT　60　(4)　312-316　2014/08

    DOI： 10.1262/jrd.2013-129 　

    ISSN： 0916-8818

  34. Microarray analysis of perinatal-estrogen-induced changes in gene expression related to brain sexual differentiation in mice Peer-reviewed

    Mototsugu Sakakibara, Yoshihisa Uenoyama, Shiori Minabe, Youki Watanabe, Chikaya Deura, Sho Nakamura, Genki Suzuki, Kei-Ichiro Maeda, Hiroko Tsukamura

    PLoS ONE　8　(11)　e79437　2013/11/04

    DOI： 10.1371/journal.pone.0079437 　

    ISSN： 1932-6203

    eISSN： 1932-6203

  35. Chronic Peripheral Administration of Kappa-Opioid Receptor Antagonist Advances Puberty Onset Associated with Acceleration of Pulsatile Luteinizing Hormone Secretion in Female Rats Peer-reviewed

    Tatsuo Nakahara, Yoshihisa Uenoyama, Akira Iwase, Shinya Oishi, Sho Nakamura, Shiori Minabe, Youki Watanabe, Chikaya Deura, Taro Noguchi, Nobutaka Fuji, Fumitaka Kikkawa, Kei-ichiro Maeda, Hiroko Tsukamura

    JOURNAL OF REPRODUCTION AND DEVELOPMENT　59　(5)　479-484　2013/10

    DOI： 10.1262/jrd.2013-046 　

    ISSN： 0916-8818

  36. Dynorphin-Kappa Opioid Receptor Signaling Partly Mediates Estrogen Negative Feedback Effect on LH Pulses in Female Rats Peer-reviewed

    Parvin Mostari, Nahoko Ieda, Chikaya Deura, Shiori Minabe, Shunji Yamada, Yoshihisa Uenoyama, Kei-ichiro Maeda, Hiroko Tsukamura

    JOURNAL OF REPRODUCTION AND DEVELOPMENT　59　(3)　266-272　2013/06

    DOI： 10.1262/jrd.2012-193 　

    ISSN： 0916-8818

  37. Different critical perinatal periods and hypothalamic sites of oestradiol action in the defeminisation of luteinising hormone surge and lordosis capacity in the rat

    M. Sakakibara, C. Deura, S. Minabe, Y. Iwata, Y. Uenoyama, K. I. Maeda, H. Tsukamura

    Journal of Neuroendocrinology　25　(3)　251-259　2013/03

    DOI： 10.1111/j.1365-2826.2012.02389.x 　

    ISSN： 0953-8194

    eISSN： 1365-2826

  38. Oestrogen-Dependent Suppression of Pulsatile Luteinising Hormone Secretion and Kiss1 mRNA Expression in the Arcuate Nucleus During Late Lactation in Rats Peer-reviewed

    S. Yamada, Y. Uenoyama, C. Deura, S. Minabe, Y. Naniwa, K. Iwata, M. Kawata, K. I. Maeda, H. Tsukamura

    Journal of Neuroendocrinology　24　(9)　1234-1242　2012/09

    DOI： 10.1111/j.1365-2826.2012.02330.x 　

    ISSN： 0953-8194 1365-2826

    eISSN： 1365-2826

  39. Epigenetic regulation of Kiss1 gene expression mediating estrogen-positive feedback action in the mouse brain Peer-reviewed

    Junko Tomikawa, Yoshihisa Uenoyama, Makiko Ozawa, Tatsuya Fukanuma, Kenji Takase, Teppei Goto, Hitomi Abe, Nahoko Ieda, Shiori Minabe, Chikaya Deura, Naoko Inoue, Makoto Sanbo, Koichi Tomita, Masumi Hirabayashi, Satoshi Tanaka, Takuya Imamura, Hiroaki Okamura, Kei-ichiro Maeda, Hiroko Tsukamura

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA　109　(20)　E1294-E1301　2012/05

    DOI： 10.1073/pnas.1114245109 　

    ISSN： 0027-8424

  40. Analysis of Pulsatile and Surge-like Luteinizing Hormone Secretion with Frequent Blood Sampling in Female Mice Peer-reviewed

    Shiori Minabe, Yoshihisa Uenoyama, Hiroko Tsukamura, Kei-ichiro Maeda

    JOURNAL OF REPRODUCTION AND DEVELOPMENT　57　(5)　660-664　2011/10

    DOI： 10.1262/jrd.11-078S 　

    ISSN： 0916-8818

Show all ︎Show first 5

Misc. 67

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    Yoichi Sutoh, Tsuyoshi Hachiya, Yayoi Otsuka-Yamasaki, Shohei Komaki, Shiori Minabe, Hideki Ohmomo, Kozo Tanno, Atsushi Hozawa, Naoki Nakaya, Mami Ishikuro, Taku Obara, Shinichi Kuriyama, Makoto Sasaki, Atsushi Shimizu

    JOURNAL OF IMMUNOLOGY　214　2025/11

    DOI： 10.1093/jimmun/vkaf283.514 　

    ISSN： 0022-1767

    eISSN： 1550-6606

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    清水厚志, 清水厚志, 小巻翔平, 小巻翔平, 荒木重則, 美辺詩織, 美辺詩織, 山崎弥生, 山崎弥生, 須藤洋一, 須藤洋一, 大桃秀樹, 大桃秀樹

    日本遺伝カウンセリング学会誌　46　(2)　2025

    ISSN： 1347-9628

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    須藤洋一, 須藤洋一, 小野加奈子, 美辺詩織, 美辺詩織, SENANAYAKE Samadhi, SENANAYAKE Samadhi, 大桃秀樹, 大桃秀樹, 八谷剛史, 八谷剛史, 清水厚志, 清水厚志, 平野雅之, 平野雅之

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  5. DNA Methylation Study in DOHaD Theory: A Perspective from the Tohoku Medical Megabank (TMM) Project Invited Peer-reviewed

    美辺詩織, 小巻翔平, 大桃秀樹, 清水厚志

    DOHad研究　12　(1)　2024/12

    ISSN： 2187-2597

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    SUTOH Yoichi, HACHIYA Tsuyoshi, OTSUKA-YAMASAKI Yayoi, TOKUTOMI Tomoharu, YOSHIDA Akiko, KOTOZAKI Yuka, KOMAKI Shohei, MINABE Shiori, OHMOMO Hideki, TANNO Kozo, FUKUSHIMA Akimune, SASAKI Makoto, SHIMIZU Atsushi

    日本人類遺伝学会大会(CD-ROM)　69th　2024

  7. 出生ゲノムコホートを用いた小児肥満リスク予測式の開発 Invited

    美辺詩織

    日本内分泌学会雑誌　100　(1)　2024

    ISSN： 0029-0661

  8. Personalized medicine through disclosing epigenomic age to individuals: Feasibility Study

    清水厚志, 小巻翔平, 荒木重則, 美辺詩織, 山崎弥生, 須藤洋一, 大桃秀樹

    日本遺伝カウンセリング学会誌　45　(2)　2024

    ISSN： 1347-9628

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    日本骨粗鬆症学会雑誌　10　(Suppl.1 (CD-ROM))　2024

    ISSN： 2189-8383

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    Clinical Neuroscience　41　(11)　2023

    ISSN： 0289-0585

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  12. 新生児臍帯血の網羅的エピゲノム解析による妊娠初期までの喫煙経験が次世代に及ぼす影響

    美辺詩織, 小巻翔平, 大桃秀樹, 高嶋聰, 小野加奈子, 山崎弥生, 須藤洋一, 田高周, 水野聖士, 石黒真美, 工藤久智, 小原拓, 熊田和貴, 勝岡史城, 荻島創一, 木下賢吾, 菅原準一, 栗山進一, 清水厚志, 清水厚志

    DOHad研究(Web)　11　(3)　2023

    ISSN： 2187-2597

  13. 発達期の栄養環境が生殖神経内分泌機構に及ぼす影響

    美辺詩織, 岩田衣世, 渡辺雄貴, 渡辺雄貴, 石井寛高, 小澤一史

    日本神経内分泌学会学術集会プログラム・抄録集　49th　2023

  14. DOHaD theory、胎児プログラミングを基軸とする環境内分泌学研究 発達期環境ストレスによる生殖機能不全をもたらす神経内分泌メカニズム

    美辺 詩織, 岩田 衣世, 渡辺 雄貴, 石井 寛高, 井上 直子, 上野山 賀久, 束村 博子, 小澤 一史

    日本内分泌学会雑誌　98　(3)　691-691　2022/07

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  15. 発達期環境ストレスと神経内分泌メカニズム

    美辺 詩織, 井上 直子, 上野山 賀久, 束村 博子, 小澤 一史

    日本内分泌学会雑誌　97　(4)　742-742　2021/12

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  16. 神経内分泌研究のアップデート 発達期エストロゲン曝露による生殖機能不全をもたらす神経内分泌メカニズム

    美辺 詩織, 井上 直子, 上野山 賀久, 小澤 一史, 束村 博子

    日本内分泌学会雑誌　97　(1)　141-141　2021/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  17. ウシ子宮内膜side population(SP)細胞の遺伝子発現解析と分娩後におけるSP細胞割合の推移

    舘林 亮輝, 中村 翔, 美辺 詩織, 古澤 軌, 阿部 良哉, 加治佐 実希, 森田 康広, 大蔵 聡, 木村 康二, 松山 秀一

    The Journal of Reproduction and Development　66　(Suppl.)　j41-j41　2020/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  18. 栄養による生殖機能・血糖・摂食調節を担うエネルギーセンサーと神経経路の同定

    佐藤 真梨萌, 美辺 詩織, 渡辺 雄貴, 後藤 哲平, 三宝 誠, 平林 真澄, 井上 直子, 上野山 賀久, 真方 文絵, 束村 博子, 松田 二子

    日本内分泌学会雑誌　95　(4)　1448-1448　2020/02

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  19. メスラットのプロラクチン分泌に及ぼすエストロゲン非依存的なニューロペプチドBの効果

    渡辺 雄貴, 美辺 詩織, 岩田 衣世, 小澤 一史

    日本内分泌学会雑誌　95　(4)　1456-1456　2020/02

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  20. ニューロペプチドBがメスラットのプロラクチン分泌に及ぼす影響

    渡辺 雄貴, 美辺 詩織, 岩田 衣世, 小澤 一史

    The Journal of Reproduction and Development　65　(Suppl.)　j96-j96　2019/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  21. ウシ子宮内膜side population細胞における幹細胞マーカーの発現解析

    舘林 亮輝, 中村 翔, 美辺 詩織, 古澤 軌, 阿部 良哉, 森田 康広, 大蔵 聡, 木村 康二, 松山 秀一

    The Journal of Reproduction and Development　65　(Suppl.)　j133-j133　2019/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  22. まき牛群での雌-雌間における生殖関連行動の経時変化

    鈴木 暁, 清川 泰志, 美辺 詩織, 武内 ゆかり

    日本獣医学会学術集会講演要旨集　162回　438-438　2019/08

    Publisher: (公社)日本獣医学会

    ISSN： 1347-8621

  23. 低栄養による性腺刺激ホルモン分泌の抑制を担う神経伝達経路とグルコースセンサーの同定

    佐藤真梨萌, 美辺詩織, 渡辺雄貴, 後藤哲平, 三宝誠, 平林真澄, 真方文絵, 束村博子, 松田二子

    Journal of Reproduction and Development　65　(Suppl Japanese Issue)　2019

    ISSN： 0916-8818

  24. 後脳上衣細胞から視床下部キスペプチンニューロンへ入力する神経経路の形態学的解析

    出浦 慎哉, 美辺 詩織, 池上 花奈, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　94　(4)　1329-1329　2018/12

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  25. 発達期雌雄ラットへのエストロジェン曝露による弓状核Kiss1抑制を介した生殖機能不全機構

    美辺 詩織, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　94　(1)　320-320　2018/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  26. 雌ウシ鋤鼻神経由来不死化細胞株の樹立

    美辺 詩織, 藤井 陽介, 松田 二子, 松山 秀一, 若林 嘉浩, 末富 祐太, 大蔵 聡, 武内 ゆかり, 前多 敬一郎

    日本畜産学会大会講演要旨集　124回　211-211　2018/03

    Publisher: (公社)日本畜産学会

    ISSN： 1342-4688

  27. ウシ子宮内膜におけるミトコンドリア機能の亢進は受胎率を飛躍的に向上させる

    松山 秀一, 中村 翔, 美辺 詩織, 岩田 尚孝, 木村 康二

    日本胚移植学雑誌　40　(1)　24-24　2018/01

    Publisher: 日本胚移植技術研究会

    ISSN： 1341-2965

  28. ウシ下垂体前葉におけるGPR120の局在

    中村翔, 中村翔, 野田航平, 野田航平, 三輪雅史, 美辺詩織, 松山秀一, 松山秀一, 森山隆太郎

    日本下垂体研究会学術集会プログラム・講演要旨集　33rd　2018

  29. 新生仔雄へのエストロジェン暴露による弓状核Kiss1抑制を介したLH分泌不全メカニズム

    美辺 詩織, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　93　(4)　1329-1329　2017/12

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  30. GnRHパルス発生機構におけるkappa-opioid receptor(KOR)発現細胞の役割

    高橋 宙大, 中村 翔, 戴 明道, 後藤 哲平, 平林 真澄, 池上 花奈, 上野山 賀久, 束村 博子, 美辺 詩織, 松田 二子, 前多 敬一郎

    日本内分泌学会雑誌　93　(4)　1333-1333　2017/12

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  31. 後脳上衣細胞のグルコースセンサー細胞としての可能性

    佐藤 真梨萌, 美辺 詩織, 渡辺 雄貴, 松田 二子, 前多 敬一郎

    日本内分泌学会雑誌　93　(4)　1334-1334　2017/12

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  32. パルス状性腺刺激ホルモン放出ホルモン(GnRH)分泌の発生メカニズムについて

    高橋 宙大, 中村 翔, 戴 明道, 後藤 哲平, 平林 真澄, 池上 花奈, 上野山 賀久, 束村 博子, 美辺 詩織, 松田 二子, 前多 敬一郎

    日本獣医学会学術集会講演要旨集　160回　441-441　2017/08

    Publisher: (公社)日本獣医学会

    ISSN： 1347-8621

  33. 摂食と生殖を制御するエネルギーセンサーとしての後脳上衣細胞

    美辺詩織, 美辺詩織, 出浦慎哉, 池上花奈, 後藤哲平, 後藤哲平, 三宝誠, 平林真澄, 井上直子, 上野山賀久, 松田二子, 束村博子, 前多敬一郎

    GPCR研究会プログラム・抄録集　14th　2017

  34. ウシ過剰排卵処置時におけるニューロキニンB受容体作動薬の静脈内投与が回収胚の発育ステージおよび遺伝子発現に及ぼす影響

    松山 秀一, 中村 翔, 美辺 詩織, 大石 真也, 大蔵 聡, 木村 康二

    日本胚移植学雑誌　39　(1)　61-61　2017/01

    Publisher: 日本胚移植技術研究会

    ISSN： 1341-2965

  35. 分娩後のウシ子宮内膜におけるSide population細胞の発現挙動

    松山 秀一, 美辺 詩織, 中村 翔, 古澤 軌, 池田 光美, 木村 康二

    The Journal of Reproduction and Development　62　(Suppl.)　j143-j143　2016/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  36. 新生仔期のエストロジェン暴露による弓状核kisspeptin抑制を介したパルス状黄体形成ホルモン(LH)分泌不全メカニズム

    美辺 詩織, 家田 菜穂子, 渡辺 雄貴, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　62　(Suppl.)　j93-j93　2016/09

    Publisher: (一社)日本繁殖生物学会

    ISSN： 0916-8818

  37. ウシ黄体におけるresistin発現制御

    伊藤 さやか, 小林 芳彦, Rak Agnieszka, 山本 ゆき, 美辺 詩織, 松山 秀一, 木村 康二, Skarzynski Dariusz J., 奥田 潔

    日本畜産学会大会講演要旨集　121回　191-191　2016/03

    Publisher: (公社)日本畜産学会

    ISSN： 1342-4688

  38. 肉用繁殖牛における分娩前の腟内温度および電気抵抗値の変動

    松山 秀一, 美辺 詩織, 吉岡 耕治, 木村 康二

    日本胚移植学雑誌　38　(1)　45-45　2016/01

    Publisher: 日本胚移植技術研究会

    ISSN： 1341-2965

  39. ウシ過剰排卵処置時におけるニューロキニンB受容体作動薬の末梢投与が黄体形成ホルモン分泌および回収胚の品質に及ぼす影響

    中村翔, 木村康二, 美辺詩織, 大石真也, 大蔵聡, 松山秀一

    Journal of Reproduction and Development　62　(Suppl Japanese Issue)　2016

    ISSN： 0916-8818

  40. キスペプチン・GnRHニューロン間のultra-short loop feedbackによるLH分泌促進機構

    家田 菜穂子, 美辺 詩織, 池上 花奈, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　61　(Suppl.)　j94-j94　2015/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  41. ウシ子宮内膜上皮細胞におけるSide population細胞の解析

    松山 秀一, 古澤 軌, 池田 光美, 美辺 詩織, 木村 康二

    The Journal of Reproduction and Development　61　(Suppl.)　j140-j140　2015/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  42. ウシにおける最終糖化産物の蓄積状況の検討

    美辺 詩織, 松山 秀一, 木村 康二

    The Journal of Reproduction and Development　61　(Suppl.)　j170-j170　2015/09

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  43. GnRHニューロンからキスペプチンニューロンへのポジティブ・ショートループ・フィードバック機構

    家田 菜穂子, 美辺 詩織, 池上 花奈, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　91　(2)　600-600　2015/09

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  44. コンディショナルKiss1KOマウスを用いたGnRHパルス発生機構の同定とKiss1可視化マウスin vitro系によるパルス発生分子メカニズムの解明

    池上 花奈, 美辺 詩織, 家田 菜穂子, 渡辺 雄貴, 後藤 哲平, 中村 翔, 井上 直子, 前多 敬一郎, 束村 博子, 上野山 賀久

    The Journal of Reproduction and Development　61　(Suppl.)　j75-j75　2015/09

    Publisher: (一社)日本繁殖生物学会

    ISSN： 0916-8818

  45. Kiss1ノックアウト雄ラットにおける生殖機能不全

    上野山 賀久, 中村 翔, 池上 花奈, 美辺 詩織, 家田 菜穂子, 冨川 順子, 後藤 哲平, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　91　(1)　298-298　2015/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  46. GnRH部分ペプチドGnRH(1-5)は弓状核キスペプチン(KNDy)ニューロンを介してLH分泌を促進する

    家田 菜穂子, 美辺 詩織, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　90　(2)　683-683　2014/09

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  47. NKB-NK3RシグナリングによるKNDyニューロンの神経活動同期メカニズム

    池上 花奈, 美辺 詩織, 家田 菜穂子, 安部 仁美, 後藤 哲平, 前多 敬一郎, 束村 博子, 上野山 賀久

    The Journal of Reproduction and Development　60　(Suppl.)　j85-j85　2014/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  48. 低栄養による繁殖抑制を担う脳内エネルギーセンシングメカニズム

    美辺 詩織, 松本 華代, 出浦 慎哉, 池上 花奈, 後藤 哲平, 三宝 誠, 平林 真澄, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　60　(Suppl.)　j86-j86　2014/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  49. キスペプチンニューロンを介したGnRH部分ペプチドによるLH分泌促進

    家田 菜穂子, 美辺 詩織, 井上 直子, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　60　(Suppl.)　j115-j115　2014/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  50. 新生児期エストロジェンにより発現が変化する視床下部内遺伝子の網羅的解析

    渡辺 雄貴, 榊原 基嗣, 上野山 賀久, 美辺 詩織, 出浦 慎哉, 中村 翔, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　60　(Suppl.)　j115-j115　2014/08

    Publisher: (一社)日本繁殖生物学会

    ISSN： 0916-8818

  51. KNDyニューロン可視化遺伝子組換えラットを用いたGnRHパルス発生機構の解明

    美辺 詩織, 林 真弓, 笹嶋 俊介, 家田 菜穂子, 後藤 哲平, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本畜産学会大会講演要旨集　118回　199-199　2014/03

    Publisher: (公社)日本畜産学会

    ISSN： 1342-4688

  52. 性成熟期の雌ブタ脳におけるKISS1遺伝子発現

    家田 菜穂子, 上野山 賀久, 難波 陽介, 渡辺 雄貴, 美辺 詩織, 冨川 順子, 井上 直子, 松田 二子, 大蔵 聡, 前多 敬一郎, 束村 博子

    日本畜産学会大会講演要旨集　118回　221-221　2014/03

    Publisher: (公社)日本畜産学会

    ISSN： 1342-4688

  53. Kiss1ノックアウト雄ラットにおけるゴナドトロピン分泌不全

    上野山 賀久, 中村 翔, 池上 花奈, 美辺 詩織, 家田 菜穂子, 冨川 順子, 後藤 哲平, 田村 千尋, 三宝 誠, 平林 真澄, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　89　(2)　593-593　2013/09

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  54. 後脳上衣細胞から視床下部への情報伝達経路の可能性

    出浦 慎哉, 美辺 詩織, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　59　(Suppl.)　j87-j87　2013/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  55. 後脳上衣細胞可視化マウスの作製

    美辺 詩織, 林 真弓, 後藤 哲平, 三寳 誠, 平林 真澄, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　59　(Suppl.)　j125-j125　2013/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  56. ラットGnRHおよびKNDy(キスペプチン、ニューロキニンB、ダイノルフィン)ニューロンに発現する受容体遺伝子の解析

    家田 菜穂子, 上野山 賀久, 美辺 詩織, 池上 花奈, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　59　(Suppl.)　j125-j125　2013/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  57. げっ歯類においてLHサージ発生機構に性差をもたらす遺伝子群の探索

    渡辺 雄貴, 榊原 基嗣, 上野山 賀久, 美辺 詩織, 出浦 慎哉, 中村 翔, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　59　(Suppl.)　j124-j124　2013/08

    Publisher: (一社)日本繁殖生物学会

    DOI： 10.14882/jrds.106.0.P-44.0 　

    ISSN： 0916-8818

  58. キスペプチンニューロンのGnRH分泌制御におけるハブニューロンとしての役割

    上野山 賀久, 中村 翔, 池上 花奈, 冨川 順子, 美辺 詩織, 後藤 哲平, 田村 千尋, 三寳 誠, 平林 真澄, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　89　(1)　229-229　2013/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  59. Kiss1ノックアウトラットを用いたキスペプチンの生殖機能制御における役割の証明

    上野山 賀久, 中村 翔, 早川 由起, 池上 花奈, 冨川 順子, 美辺 詩織, 後藤 哲平, 家田 菜穂子, 田村 千尋, 三寳 誠, 平林 真澄, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　88　(2)　640-640　2012/09

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  60. キスペプチンニューロンは興奮性アミノ酸によるGnRH/LH分泌刺激を仲介する

    上野山 賀久, 中村 翔, 早川 由起, 池上 花奈, 冨川 順子, 美辺 詩織, 後藤 哲平, 家田 菜穂子, 田村 千尋, 三寳 誠, 平林 真澄, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　88　(2)　746-747　2012/09

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  61. Kiss1ノックアウトラットを用いた繁殖機能制御におけるキスペプチンの役割の証明

    中村 翔, 上野山 賀久, 早川 由紀, 池上 花奈, 冨川 順子, 美辺 詩織, 後藤 哲平, 家田 菜穂子, 田村 千尋, 三宝 誠, 平林 真澄, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　58　(Suppl.)　j90-j90　2012/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

  62. 腟内留置型プロジェステロン製剤(PRID)を用いたブタの発情同期化

    中田 智子, 星野 佑太, 田島 瑶子, 上田 淳一, 難波 陽介, 美辺 詩織, 上野山 賀久, 束村 博子, 大蔵 聡, 前多 敬一郎, 野口 倫子, 鈴木 千恵, 吉岡 耕治

    日本養豚学会誌 = The Japanese journal of swine science　49　(2)　79-79　2012/06/25

    ISSN： 0913-882X

  63. マウスにおけるパルス状およびサージ状黄体形成ホルモン分泌解析

    美辺 詩織, 出浦 慎哉, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　88　(1)　267-267　2012/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  64. Kiss1-floxedマウスを用いた弓状核キスペプチンニューロンの機能解析

    中村 翔, 柳原 萌, 平嶋 昂, 美辺 詩織, 出浦 慎哉, 家田 菜穂子, 後藤 哲平, 深沼 達也, 今村 拓也, 三宝 誠, 冨田 江一, 平林 真澄, 冨川 順子, 上野山 賀久, 束村 博子, 前多 敬一郎

    日本内分泌学会雑誌　88　(1)　344-344　2012/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  65. 成体雌ラットにおいてダイノルフィンがGnRH/LHパルスに対するエストロゲンのnegative feedbackに与える影響(Involvement of dynorphin in estrogen negative feedback on GnRH/LH pulses in adult female rats)

    モスタリ・パラヴィン, 家田 菜穂子, 出浦 慎也, 美辺 詩織, 富川 順子, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　88　(1)　344-344　2012/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  66. 第4脳室周囲上衣細胞からのシグナル伝達の可能性

    出浦 慎哉, 美辺 詩織, 上野山 賀久, 前多 敬一郎, 束村 博子

    日本内分泌学会雑誌　88　(1)　344-344　2012/04

    Publisher: (一社)日本内分泌学会

    ISSN： 0029-0661

    eISSN： 2186-506X

  67. 様々な条件下のマウスにおけるパルス状LH分泌

    美辺 詩織, 上野山 賀久, 前多 敬一郎, 束村 博子

    The Journal of Reproduction and Development　56　(Suppl.)　j82-j82　2010/08

    Publisher: (公社)日本繁殖生物学会

    ISSN： 0916-8818

    eISSN： 1348-4400

Show all ︎Show first 5

Books and Other Publications 1

  1. 疾患原因遺伝子・タンパク質の 解析技術と創薬/診断技術への応用

    美辺詩織, 小巻翔平, 清水厚志

    技術情報協会　2022/03/31

    ISBN: 9784861048777

Presentations 31

  1. 低インプットDNAメチル化解析手法の確立と Avida Methyl Reagent Kitによる新たな可能性 Invited

    美辺詩織, 大桃秀樹, 清水厚志

    第18回日本エピジェネティクス研究会年会　2025/06/19

  2. 出生ゲノムコホートを用いた小児肥満リスク予測式の開発 Invited

    美辺詩織

    第97回日本内分泌学会学術総会　2024/06/06

  3. 発達期の栄養環境が生殖神経内分泌機構に及ぼす影響 Invited

    美辺詩織, 岩田衣世, 渡辺雄貴, 石井寛高, 小澤一史

    第49回日本神経内分泌学会学術集会　2023/10/28

  4. 新生児臍帯血の網羅的エピゲノム解析による妊娠初期までの喫煙経験が次世代に及ぼす影響

    美辺詩織, 小巻翔平, 大桃秀樹, 高嶋聰, 小野加奈子, 山﨑弥生, 須藤洋一, 田高周, 水野聖士, 石黒真美, 工藤久智, 小原拓, 熊田和貴, 勝岡史城, 荻島創一, 木下賢吾, 菅原準一, 栗山進一, 清水厚志

    第11回日本DOHaD学会学学術集会　2023/08/05

  5. iMETHYLの使い方 Invited

    美辺詩織

    第７回ゲノムコホート研究における遺伝統計学セミナー　2023/01

  6. TMM三世代コホートを用いたエピゲノム世代継承の証明にむけて Invited

    美辺詩織

    子どものこころの分子制御機構研究センター令和4年度連続セミナー第6回　2022/12

  7. 発達期環境ストレスによる生殖機能不全をもたらす神経内分泌メカニズム Invited

    美辺詩織, 岩田衣世, 渡辺雄貴, 石井寛高, 井上直子, 上野山賀久, 束村博子, 小澤一史

    日本内分泌学会第 40 回内分泌代謝学サマーセミナー　2022/07

  8. 発達期環境ストレスと神経内分泌メカニズム Invited

    美辺 詩織, 井上 直子, 上野山 賀久, 束村 博子, 小澤 一史

    第22回日本内分泌学会関東甲信越支部学術集会　2021/09

  9. 発達期エストロゲン曝露による生殖機能不全をもたらす神経内分泌メカニズム Invited

    美辺詩織, 井上直子, 上野山賀久, 小澤一史, 束村博子

    第94回日本内分泌学会学術総会　2021/04

  10. 発達期雌雄ラットへのエストロジェン曝露による弓状核Kiss1抑制を介した生殖機能不全機構

    美辺詩織, 井上直子, 上野山賀久, 前多敬一郎, 束村博子

    第91回日本内分泌学会学術総会　2018/04

  11. Neonatal chronic exposure to estrogen inhibits LH pulses by suppressing arcuate Kiss1 expression in male rats International-presentation

    Minabe, S, Sato, M, Inoue, N, Uenoyama, Y, Maeda, K, Tsukamura, H

    ENDO2018　2018/03

  12. 雌ウシ鋤鼻神経由来不死化細胞株の樹立

    美辺詩織, 藤井陽介, 松田二子, 松山秀一, 若林嘉浩, 末富祐太, 大蔵聡, 武内ゆかり, 前多敬一郎

    日本畜産学会第124回大会　2018/03

  13. Kisspeptin neurons in the arcuate nucleus is a target of estrogen in developing brain to lead reproductive toxicity in male rats International-presentation

    Minabe, S, Inoue, N, Uenoyama, Y, Maeda, K, Tsukamura, H

    4th World Congress on Reproductive Biology　2017/09

  14. 新生仔期のエストロジェン暴露による弓状核kisspeptin抑制を介したパルス状黄体形成ホルモン（LH）分泌不全メカニズム

    美辺詩織, 家田菜穂子, 渡辺雄貴, 上野山賀久, 前多敬一郎, 束村博子

    第109回日本繁殖生物学会大会　2017/09

  15. 新生仔雄へのエストロジェン暴露による弓状核Kiss1抑制を介したLH分泌不全メカニズム

    美辺詩織, 井上直子, 上野山賀久, 前多敬一郎, 束村博子

    第22回生殖内分泌学会学術集会　2017/09

  16. 摂食と生殖を制御するエネルギーセンサーとしての後脳上衣細胞の役割

    美辺詩織, 出浦慎哉, 池上花奈, 後藤哲平, 三宝誠, 平林真澄, 井上直子, 上野山賀久, 佐藤真梨萌, 松田二子, 束村博子, 前多敬一郎

    第2回食欲・食嗜好の分子・神経基盤研究会　2017/06

  17. 摂食と生殖を制御するエネルギーセンサーとしての後脳上衣細胞

    美辺詩織, 出浦慎哉, 池上花奈, 後藤哲平, 三宝誠, 平林真澄, 井上直子, 上野山賀久, 松田二子, 束村博子, 前多敬一郎

    第14回GPCR研究会　2017/05

  18. Long-term neonatal exposure to estrogen inhibits LH pulses by suppressing arcuate Kiss1 expression via estrogen receptor α in female rodents International-presentation

    Minabe, S, Ieda, N, Watanabe, Y, Inoue, N, Uenoyama, Y, Maeda, K, Tsukamura, H

    ENDO2017　2017/03

  19. 低栄養による繁殖抑制を担う脳内エネルギーセンシングメカニズム

    美辺詩織, 松本華代, 出浦慎哉, 池上花奈, 後藤哲平, 三宝誠, 平林真澄, 上野山賀久, 前多敬一郎, 束村博子

    第107回日本繁殖生物学会大会　2016/09

  20. ウシにおける最終糖化産物の蓄積状況の検討

    美辺詩織, 松山秀一, 木村康二

    第108回日本繁殖生物学会大会　2015/09

  21. Energy sensing mechanism in the brain to mediate suppression of reproduction under malnutrition

    Minabe S, Matsumoto K, Deura C, Ikegami K, Goto T, Sanbo M, Hirabayashi M, Uenoyama Y, Maeda K, Tsukamura H

    第107回日本繁殖生物学会大会　2014/08

  22. 性腺機能制御に関わる後脳上衣細胞のAMP活性化プロテインキナーゼ（AMPK）の役割

    美辺詩織, 松本華代, 出浦慎哉, 池上花奈, 後藤哲平, 三宝誠, 平林真澄, 上野山賀久, 前多敬一郎, 束村博子

    日本下垂体研究会第29回学術集会　2014/08

  23. KNDyニューロン可視化遺伝子組換えラットを用いたGnRHパルス発生機構の解明

    美辺詩織, 林真弓, 笹嶋俊介, 家田菜穂子, 後藤哲平, 上野山賀久, 前多敬一郎, 束村博子

    日本畜産学会第118回大会　2014/03

  24. 後脳上衣細胞可視化マウスの作製

    美辺詩織, 林真弓, 後藤哲平, 三宝誠, 平林真澄, 上野山賀久, 前多敬一郎, 束村博子

    第106回日本繁殖生物学会大会　2013/09

  25. Analysis of Luteinizing Hormone Pulse and Surge in Female Mice International-presentation

    Minabe S, Deura C, Uenoyama Y, Maeda K, Tsukamura H

    2nd World Conference on Kisspeptin Signaling in the Brain　2012/11

  26. Generation of transgenic mice with vimentin-driven reporter fluorescence in the ependymocytes International-presentation

    Minabe S, Deura C, Goto T, Sanbo M, Tomita K, Hirabayashi M, Uenoyama Y, Tsukamura H, Maeda K

    Neurosceience2012　2012/10

  27. 後脳上衣細胞レポーター遺伝子導入マウスの作製

    美辺詩織, 上野山賀久, 前多敬一郎, 束村博子

    日本下垂体研究会第27回学術集会　2012/08

  28. マウスにおけるパルス状およびサージ状黄体形成ホルモン分泌解析

    美辺詩織, 上野山賀久, 前多敬一郎, 束村博子

    第85回日本内分泌学会学術総会　2012/04

  29. マウスを用いた連続採血法の確立—小さい体に秘めた大きな可能性

    美辺詩織, 出浦慎哉, 上野山賀久, 前多敬一郎, 束村博子

    名古屋大学若手女性研究者サイエンスフォーラム　2011/11

  30. Luteinizing Hormone Pulse and Surge in Female ICR Mice International-presentation

    Minabe S, Uenoyama Y, Tsukamura H, Maeda K

    World Congress on Reproductive Biology　2011/10

  31. マウス頻回採血法の確立

    美辺詩織, 上野山賀久, 前多敬一郎, 束村博子

    第103回日本繁殖生物学会大会　2010/08

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Research Projects 9

  1. Deciphering non-genetic epigenetic inheritance: A three-generation multi-omics approach in a Japanese population

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research (C)

    Institution: Tohoku University

    2026/04/01 - 2029/03/31

  2. ３世代7人家族の網羅的DNAメチル化解析によるエピゲノム世代継承の証明

    美辺 詩織

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 若手研究

    Category: 若手研究

    Institution: 岩手医科大学

    2023/04/01 - 2026/03/31

  3. 出生ゲノムコホートを用いた小児肥満リスク予測式の開発

    Offer Organization: 日本内分泌学会

    System: 日本内分泌学会研究助成制度（若手研究者による研究課題）

    Category: 臨床・内科以外

    Institution: いわて東北メディカル・メガバンク機構 生体情報解析部門

    2023/04 - 2024/03

  4. Neuroendocrine mechanism of precocious puberty caused by fetal stress in utero

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Early-Career Scientists

    2020/04/01 - 2023/03/31

  5. 肥満を基盤とした生殖機能低下を惹起する神経内分泌メカニズムと脳内神経炎症の相関

    美辺 詩織

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 特別研究員奨励費

    Category: 特別研究員奨励費

    Institution: 日本医科大学

    2020/04 - 2023/03

    More details Close

    肥満関連疾患のひとつに不妊症があり、BMIが増加すると妊娠率は低下、排卵障害は増加する。過栄養による生殖機能低下は種間で保存された現象であるが、その 詳細な発症機序は不明である。本研究では、肥満が哺乳類の生殖中枢であるキスペプチンニューロンに及ぼす影響に着目し、肥満を基盤とした生殖機能低下を惹起する視床下部の病態と発症機序について神経内分泌メカニズムの全容解明を目的とする。本研究は、欧米先進国や東南アジア新興国における肥満を基盤とした不妊症や、日本における代謝異常に伴った排卵障害の発症メカニズムを説明するものである。実験では、4ヶ月間の高脂肪食給餌により肥満を誘導した雌雄ラットを用いて、肥満が生殖機能に及ぼす影響を評価した。雄ラットでは肥満により弓状核のキスペプチン 遺伝子(Kiss1)発現が抑制された。一方、雌ラットでは肥満による血中エストロゲン濃度低下、子宮重量の低下や性周期異常が観察されたものの、ゴナドトロピン(LH)及びKiss1発現は対象群と差はなかった。このことから、雌では肥満によりゴナドトロピン非依存的に卵巣の性ステロイド合成が阻害されると考えられる。さらに、雌と比較して雄のKiss1発現低下が早期に起こることから、食事性肥満に対するキスペプチンニューロンの感受性には雌雄差があることが示唆された。これらの研究成果をまとめた学術論文はPeptide誌に受理され、2021年8月号に掲載された。なお、採用から1年3ヶ月で所属異動により特別研究員は中途辞退した。

  6. 肥満を基盤とした不妊を惹起する神経内分泌メカニズムの解明

    Offer Organization: 日本医科大学

    System: 2019年度 若手・女性研究者奨励助成金

    2019 - 2020

  7. 繁殖機能の制御に関わる脳内グルコースセンシングメカニズムの解明 Competitive

    美辺 詩織

    Offer Organization: 財団法人日本科学協会

    System: 笹川科学研究助成

    2017/04 - 2018/03

  8. Identification of energy sensors mediating suppression of reproductive functions under malnutrition

    Maeda Kei-ichiro

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Category: Grant-in-Aid for Scientific Research (B)

    Institution: The University of Tokyo

    2012/04/01 - 2016/03/31

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    In lactating cows, gonadal functions are suppressed because of the malnutrition caused by a big milk yield. The suppression is probably due to a decrease in energy levels. Hindbrain ependymocyte is a candidate for energy sensor involved in the suppression of gonadal activities through suppressing gonadotropin secretion in rats. We aimed to get evidence for ependymocytes to sense glucose levels through AMP kinase which is considered to be a energy-sensing molecule in various kinds of cells. In addition, a neural pathway relaying information on the energy level from ependymocytes to the hypothalamic neurons controlling reproduction. As a result, ependymocytes senses extracellular glucose levels through an AMP kinase-mediated mechanism. In addition, the information on energy level might be transmitted from ependymocytes to neurons located in the hypothalamic paraventricular nucleus. The present result would contribute to treatments of reproductive disorders in lactating cows.

  9. 遺伝子欠損モデルを用いた生殖を制御する新規エネルギーセンサー細胞の同定

    美辺 詩織

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 特別研究員奨励費

    Category: 特別研究員奨励費

    Institution: 名古屋大学

    2012/04 - 2015/03

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    本研究では、上衣細胞におけるエネルギーセンシングの細胞内シグナリングを解明することを目的として、後脳上衣細胞のAMP活性化プロテインキナーゼ（AMPK）の役割について検討した。AMPKは真核細胞において高度に保存されているセリン／スレオニンキナーゼであり、低グルコースのような低栄養ストレスに応答してAMP依存的に活性化される。本研究において、後脳の細胞のなかでも特に脳室周囲の上衣細胞の繊毛にAMPKタンパクの局在が示された。また、AMPKの活性化剤をラット後脳に位置する第四脳室に投与すると、パルス状LH分泌が抑制されたことから、上衣細胞の繊毛のAMPK活性化が性腺機能を抑制することが示唆された。さらに、上衣細胞で蛍光タンパク質（Venus）を発現するトランスジェニックマウスを作出し、in vitroにおいてVenusで可視化された後脳上衣細胞にAMPKの活性化剤を作用させると、細胞内Ca2+濃度が上昇する。以上の結果から、後脳上衣細胞はAMPKの活性化による細胞内Ca2+濃度上昇を介してパルス状LH分泌の抑制を引き起こすことが示唆された。これまでニューロンの支持細胞と考えられていたグリア細胞であるが、近年の多くの研究から、実は非常に動的であり、細胞内Ca2+濃度に依存的にさまざまな伝達物質を放出することが報告されている。これらのことから、低栄養時には、エネルギーセンサー細胞である後脳上衣細胞内の細胞内AMPKシグナリングの活性化が引き金となり、視床下部の生殖中枢へと低栄養の情報が伝達され、GnRH/LH 分泌を抑制し、ひいては性腺機能を抑制すると考えられる。本研究により明らかとなった性腺機能を制御する脳内エネルギーセンシングメカニズムは、高泌乳牛における受胎率の低下などに関わる可能性が考えられ、治療・予防法の開発への応用が期待される。

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Social Activities 3

  1. 日本繁殖生物学会大会 若手企画

    2015 - 2017

  2. 日本畜産学会 第124回大会 実行委員

    2018/03 -

  3. 日本神経内分泌学会 神経内分泌テクニカルスクール

    2017/11 -