Details of the Researcher

PHOTO

Yuta Chiba
Section
Graduate School of Dentistry
Job title
Senior Assistant Professor
Degree
e-Rad No.
10821986
Profile

日本小児歯科学会専門医

日本小児歯科学会専門医指導医

Research History 14

  • 2024/08 - Present
    東北大学大学院歯学研究科　小児発達歯科学分野　講師

  • 2024/01 - 2024/07
    Tohoku University

  • 2022/11 - 2023/12
    （併）東北大学大学院歯学研究科　小児発達歯科学分野　非常勤講師

  • 2022/09 - 2023/12
    （併）厚生労働省　東北厚生局 復興支援本部

  • 2022/09 - 2023/12
    厚生労働省　東北厚生局 健康福祉部 医事課　課長

  • 2022/09 - 2023/12
    （併）厚生労働省　大臣官房 厚生科学課 健康危機管理・災害対策室

  • 2021/04 - 2022/08
    （併）九州大学大学院歯学研究院　歯学発生再生(DDR)センター

  • 2021/02 - 2022/08
    九州大学大学院歯学研究院　小児口腔医学分野　助教

  • 2020/04 - 2021/01
    Tohoku University

  • 2019/04 - 2020/03
    東北大学病院　小児歯科　特任助手

  • 2018/04 - 2019/03
    東北大学病院　小児歯科　医員

  • 2015/04 - 2018/03
    日本学術振興会　特別研究員（DC1）

  • 2016/01 - 2018/01
    National Institutes of Health　NIDCR　Graduate Partnership Program Research Fellow

  • 2013/04 - 2014/03
    東北大学病院歯科医師臨床研修プログラム　研修医

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Education 2

  • 東北大学大学院歯学研究科 小児発達歯科学分野 博士課程

    2014 - 2018

  • Tohoku University　Faculty of Dentistry

    2007 - 2013

Committee Memberships 4

  • 日本小児歯科学会　北日本地方会 常任幹事

    2026/04 - Present

  • 日本小児歯科学会　研究倫理審査委員会

    2024/08 - Present

  • 日本小児歯科学会　診療ガイドライン委員会

    2024/06 - Present

  • 東北大学病院　小児歯科医局長

    2024/04 - Present

Professional Memberships 5

  • 日本口腔衛生学会

    2026/07 -

  • 日本障害者歯科学会

    2021/04 -

  • JAPANESE ASSOCIATION FOR ORAL BIOLOGY

    2018/04 -

  • International Association for Dental Research

    2017/03 -

  • THE JAPANESE SOCIETY OF PEDIATRIC DENTISTRY

    2012/12 -

Research Interests 6

  • Dental anomaly

  • Tooth development

  • 障害者歯科学

  • 細胞生物学

  • 分子生物学

  • 小児歯科学

Research Areas 3

  • Life sciences / Cell biology /

  • Life sciences / Molecular biology /

  • Life sciences / Developmental dentistry /

Awards 8

  1. Pediatric Dental Journal 優秀論文賞

    2026/05

  2. 日本小児歯科学会 最優秀発表賞 "SHOFU AWARD"

    2025/05

  3. アジア小児歯科学会 最優秀口演発表賞

    2024/11

  4. 日本小児歯科学会 学術賞 "LION AWARD"

    2024/05

  5. Pediatric Dental Journal 優秀論文賞

    2023/05

  6. 日本小児歯科学会 奨励賞

    2021/05

  7. アジア小児歯科学会 最優秀ポスター発表賞

    2018/09

  8. 日本小児歯科学会 優秀発表賞

    2018/05

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Papers 44

  1. Nephronectin promotes ameloblast differentiation through its RGD motif Peer-reviewed

    Kanji Mizuta, Yuta Chiba, Tian Tian, Shao Shuai, Natsuki Kozai, Ichiro Takahashi, Satoshi Fukumoto, Keigo Yoshizaki

    Biochemical and Biophysical Research Communications　2026/09

    DOI： 10.1016/j.bbrc.2026.154409 　

  2. Case Report: Exploring the link between severe gingivitis and inflammatory bowel disease in a young patient Peer-reviewed

    Maruya, Yuriko, Hoshikawa, Seira, Fujiogi, Momoko, Tsuruta, Yuma, Hino, Ryoko, Tadano, Manami, Otake, Shinji, Chiba, Yuta, Yamada, Aya, Fukumoto, Satoshi, Saito, Kan

    Frontiers in Dental Medicine　2026/05

    DOI： 10.3389/fdmed.2026.1744911 　

    ISSN： 2673-4915

  3. Keratin 15 Regulates Cell Proliferation in Outer Enamel Epithelium Peer-reviewed

    Y. Chiba, T. Tian, K. Yoshizaki, X. Wang, A. Yamada, S. Fukumoto

    Journal of Dental Research　2026/05

    DOI： 10.1177/00220345251368346 　

  4. AmeloD regulates cell proliferation and differentiation process of ameloblasts through modulation of the sonic hedgehog (shh) signaling pathway Peer-reviewed

    Sae Oka, Yuta Chiba, Hiroshi Sato, Mistuki Chiba, Itaru Komine, Yuta Hirofuji, Aya Yamada, Satoshi Fukumoto

    Journal of Oral Biosciences　2026/04

    DOI： 10.1016/j.job.2026.100758 　

  5. Identifying cell-type-specific marker genes of dental epithelial cells using single-cell RNA sequence: A review Invited Peer-reviewed

    Triana Marchelina, Yuta Chiba, Keigo Yoshizaki, Satoshi Fukumoto

    Journal of Oral Biosciences　2026/02

    DOI： 10.1016/j.job.2026.100757 　

  6. Identification of a desmocollin 3–β-catenin complex modulated by Vwde–calpain signaling in ameloblast differentiation Peer-reviewed

    Yumiko Nakashima, Kokoro Iwata, Asuna Sugimoto, Manami Tanaka, Muhammad Dhiaulfikri Nauval Hadiana, Nodoka Ato, Atsushi Oishi, Kanae Wada, Yuta Chiba, Triana Marchelina, Aya Yamada, Satoshi Fukumoto, Akihito Yamamoto, Tsutomu Iwamoto

    Biochemical and Biophysical Research Communications　2025/12

    DOI： 10.1016/j.bbrc.2025.153000 　

  7. Enamel protection in pediatric patients using a bracket bonding agent with a bioactive monomer Peer-reviewed

    Manami Tadano, Ryoko Hino, Seira Hoshikawa, Yuma Tsuruta, Shinji Otake, Yuta Chiba, Aya Yamada, Satoshi Fukumoto, Yuriko Maruya, Kan Saito

    Pediatric Dental Journal　2025/12

    DOI： 10.1016/j.pdj.2025.100368 　

  8. Expression patterns of desmosome family members during tooth development and the role of Desmocollin-3 in cytodifferentiation of stratum intermedium Peer-reviewed

    Triana Marchelina, Yuta Chiba, Shinji Otake, Li Wanshu, Hiroshi Sato, Yumiko Nakashima, Asuna Sugimoto, Tsutomu Iwamoto, Aya Yamada, Kan Saito, Satoshi Fukumoto

    Archives of Oral Biology　2025/12

    DOI： 10.1016/j.archoralbio.2025.106404 　

  9. Characterization of gene expression profile of dental pulp stem cells from human exfoliated deciduous teeth (SHED) in down syndrome Peer-reviewed

    Itaru Komine, Yuta Chiba, Hiroshi Sato, Sae Oka, Keigo Yoshizaki, Aya Yamada, Satoshi Fukumoto

    Pediatric Dental Journal　2025/12

    DOI： 10.1016/j.pdj.2025.100360 　

  10. Integration of single cell analysis of dental mesenchyme and human disease database identifies the responsible gene of dentin disorders Peer-reviewed

    Hidenori Kokubo, Yuta Chiba, Triana Marchelina, Kifu Miyata, Hidenori Oikawa, Rion Sho, Kan Saito, Aya Yamada, Satoshi Fukumoto

    Pediatric Dental Journal　2025/04

    DOI： 10.1016/j.pdj.2024.100337 　

  11. Case Report: Dental treatment under general anesthesia and dental management of a child with congenital ichthyosis Peer-reviewed

    Ryoko Hino, Yuta Chiba, Yuriko Maruya, Manami Tadano, Shinji Otake, Seira Hoshikawa, Yoji Sasahara, Kan Saito

    Frontiers in Dental Medicine　5　2024/10/17

    Publisher: Frontiers Media SA

    DOI： 10.3389/fdmed.2024.1481658 　

    eISSN： 2673-4915

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    Congenital ichthyosis is a disease in which the stratum corneum on the surface of the skin becomes thick from the time of the fetus and the barrier function of the skin is impaired. Congenital ichthyosis is a genetic disorder that causes ectodermal abnormalities and sometimes affects skin, nails, and tooth enamel. Therefore, some patients require special care in their daily life and during dental treatments. Here, the authors report a case of congenital ichthyosis that developed into severe dental caries at two years and nine months of age. The authors performed whole-exome sequencing in his peripheral blood and found that the patient had compound heterozygous mutations in ALOX12B gene (c.159C>G and c.1579G>A), which is responsible for autosomal recessive congenital ichthyosis-2 (MIM#2421000). Mutation of c.159C>G is a nonsense mutation that has never been reported, therefore novel symptoms might have found. The patients exhibited severe caries by hypoplastic teeth. Here, the authors report the treatment of dental caries in a patient with congenital ichthyosis under general anesthesia and its oral management until mixed dentition.

  12. Orthodontic management of severe inversely impacted maxillary central incisors: a case series Peer-reviewed

    Yuriko Maruya, Ryoko Hino, Manami Tadano, Seira Hoshikawa, Shinji Otake, Yuta Chiba, Kan Saito

    Frontiers in Oral Health　5　2024/10/16

    Publisher: Frontiers Media SA

    DOI： 10.3389/froh.2024.1474190 　

    eISSN： 2673-4842

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    Background Abnormal positioning and dislocation of the central incisor can disturb tooth eruption. Generally, inversely impacted maxillary central incisors do not erupt naturally. Performing traction and applied extrusion of an inversely impacted maxillary central incisor with a high inclination angle of the crown is challenging. This study aimed to examine the possibility of orthodontic treatment for severely inversely impacted maxillary central incisors in a series of case studies. Methods The inclination angle of the tooth crown, curvature of the tooth root, and length of the formed tooth root were measured using radiography. The teeth were then fenestrated and traction was applied using a lingual arch appliance with elastics. Results The average crown axis inclination was 113°, the degree of root curvature was 97.3°, and the root formation was 36.1%. Although the crown axis inclination and root curvature were severe, all the incisors were aligned in the correct position as vital teeth through surgical and orthodontic treatments. Conclusions Traction should be performed in the early period of incisor development when root formation is not progressing, regardless of the tooth angle.

  13. Expression patterns of keratin family members during tooth development and the role of keratin 17 in cytodifferentiation of stratum intermedium and stellate reticulum. International-journal Peer-reviewed

    Saori Inada, Yuta Chiba, Tian Tian, Hiroshi Sato, Xin Wang, Keigo Yoshizaki, Sae Oka, Aya Yamada, Satoshi Fukumoto

    Journal of cellular physiology　e31387　2024/07/16

    DOI： 10.1002/jcp.31387 　

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    Keratins are typical intermediate filament proteins of the epithelium that exhibit highly specific expression patterns related to the epithelial type and stage of cellular differentiation. They are important for cytoplasmic stability and epithelial integrity and are involved in various intracellular signaling pathways. Several keratins are associated with enamel formation. However, information on their expression patterns during tooth development remains lacking. In this study, we analyzed the spatiotemporal expression of keratin family members during tooth development using single-cell RNA-sequencing (scRNA-seq) and microarray analysis. scRNA-seq datasets from postnatal Day 1 mouse molars revealed that several keratins are highly expressed in the dental epithelium, indicating the involvement of keratin family members in cellular functions. Among various keratins, keratin 5 (Krt5), keratin 14 (Krt14), and keratin 17 (Krt17) are highly expressed in the tooth germ; KRT17 is specifically expressed in the stratum intermedium (SI) and stellate reticulum (SR). Depletion of Krt17 did not affect cell proliferation in the dental epithelial cell line SF2 but suppressed their differentiation ability. These results suggest that Krt17 is essential for SI cell differentiation. Furthermore, scRNA-seq results indicated that Krt5, Krt14, and Krt17 exhibited distinct expression patterns in ameloblast, SI, and SR cells. Our findings contribute to the elucidation of novel mechanisms underlying tooth development.

  14. S100a6 knockdown promotes the differentiation of dental epithelial cells toward the epidermal lineage instead of the odontogenic lineage Peer-reviewed

    Shinji Otake, Kan Saito, Yuta Chiba, Aya Yamada, Satoshi Fukumoto

    The FASEB Journal　2024/04/15

    DOI： 10.1096/fj.202302412RR 　

  15. Arl4c is involved in tooth germ development through osteoblastic/ameloblastic differentiation International-journal Peer-reviewed

    Thinh Thi Kim Truong, Shinsuke Fujii, Ryoko Nagano, Kana Hasegawa, Megumi Kokura, Yuta Chiba, Keigo Yoshizaki, Satoshi Fukumoto, Tamotsu Kiyoshima

    Biochemical and Biophysical Research Communications　679　167-174　2023/09

    DOI： 10.1016/j.bbrc.2023.09.014 　

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    Murine tooth germ development proceeds in continuous sequential steps with reciprocal interactions between the odontogenic epithelium and the adjacent mesenchyme, and several growth factor signaling pathways and their activation are required for tooth germ development. The expression of ADP-ribosylation factor (Arf)-like 4c (Arl4c) has been shown to induce cell proliferation, and is thereby involved in epithelial morphogenesis and tumorigenesis. In contrast, the other functions of Arl4c (in addition to cellular growth) are largely unknown. Although we recently demonstrated the involvement of the upregulated expression of Arl4c in the proliferation of ameloblastomas, which have the same origin as odontogenic epithelium, its effect on tooth germ development remains unclear. In the present study, single-cell RNA sequencing (scRNA-seq) analysis revealed that the expression of Arl4c, among 17 members of the Arf-family, was specifically detected in odontogenic epithelial cells, such as those of the stratum intermedium, stellate reticulum and outer enamel epithelium, of postnatal day 1 (P1) mouse molars. scRNA-seq analysis also demonstrated the higher expression of Arl4c in non-ameloblast and inner enamel epithelium, which include immature cells, of P7 mouse incisors. In the mouse tooth germ rudiment culture, treatment with SecinH3 (an inhibitor of the ARNO/Arf6 pathway) reduced the size, width and cusp height of the tooth germ and the thickness of the eosinophilic layer, which would involve the synthesis of dentin and enamel matrix organization. In addition, loss-of-function experiments using siRNAs and shRNA revealed that the expression of Arl4c was involved in cell proliferation and osteoblastic cytodifferentiation in odontogenic epithelial cells. Finally, RNA-seq analysis with a gene set enrichment analysis (GSEA) and Gene Ontology (GO) analysis showed that osteoblastic differentiation-related gene sets and/or GO terms were downregulated in shArl4c-expressing odontogenic epithelial cells. These results suggest that the Arl4c-ARNO/Arf6 pathway axis contributes to tooth germ development through osteoblastic/ameloblastic differentiation.

  16. Deficiency of G protein-coupled receptor Gpr111/Adgrf2 causes enamel hypomineralization in mice by alteration of the expression of kallikrein-related peptidase 4 (Klk4) during pH cycling process. International-journal Peer-reviewed

    Yuta Chiba, Keigo Yoshizaki, Hiroshi Sato, Tomoko Ikeuchi, Craig Rhodes, Mitsuki Chiba, Kan Saito, Takashi Nakamura, Tsutomu Iwamoto, Aya Yamada, Yoshihiko Yamada, Satoshi Fukumoto

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology　37　(4)　e22861　2023/04

    DOI： 10.1096/fj.202202053R 　

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    Enamel is formed by the repetitive secretion of a tooth-specific extracellular matrix and its decomposition. Calcification of the enamel matrix via hydroxyapatite (HAP) maturation requires pH cycling to be tightly regulated through the neutralization of protons released during HAP synthesis. We found that Gpr115, which responds to changes in extracellular pH, plays an important role in enamel formation. Gpr115-deficient mice show partial enamel hypomineralization, suggesting that other pH-responsive molecules may be involved. In this study, we focused on the role of Gpr111/Adgrf2, a duplicate gene of Gpr115, in tooth development. Gpr111 was highly expressed in mature ameloblasts. Gpr111-KO mice showed enamel hypomineralization. Dysplasia of enamel rods and high carbon content seen in Gpr111-deficient mice suggested the presence of residual enamel matrices in enamel. Depletion of Gpr111 in dental epithelial cells induced the expression of ameloblast-specific protease, kallikrein-related peptidase 4 (Klk4), suggesting that Gpr111 may act as a suppressor of Klk4 expression. Moreover, reduction of extracellular pH to 6.8 suppressed the expression of Gpr111, while the converse increased Klk4 expression. Such induction of Klk4 was synergistically enhanced by Gpr111 knockdown, suggesting that proper enamel mineralization may be linked to the modulation of Klk4 expression by Gpr111. Furthermore, our in vitro suppression of Gpr111 and Gpr115 expression indicated that their suppressive effect on calcification was additive. These results suggest that both Gpr111 and Gpr115 respond to extracellular pH, contribute to the expression of proteolytic enzymes, and regulate the pH cycle, thereby playing important roles in enamel formation.

  17. Identification of GPI-anchored protein LYPD1 as an essential factor for odontoblast differentiation in tooth development. International-journal Peer-reviewed

    Yao Fu, Kanako Miyazaki, Yuta Chiba, Keita Funada, Tomomi Yuta, Tian Tian, Kanji Mizuta, Jumpei Kawahara, Ling Zhang, Daniel Martin, Tsutomu Iwamoto, Ichiro Takahashi, Satoshi Fukumoto, Keigo Yoshizaki

    The Journal of biological chemistry　104638-104638　2023/03/22

    DOI： 10.1016/j.jbc.2023.104638 　

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    Lipid rafts are membrane microdomains rich in cholesterol, sphingolipids, glycosylphosphatidylinositol-anchored proteins (GPI-APs), and receptors. These lipid raft components are localized at the plasma membrane and are essential for signal transmission and organogenesis. However, few reports have been published on the specific effects of lipid rafts on tooth development. Using microarray and single-cell RNA sequencing methods, we found that a GPI-AP, lymphocyte antigen-6 (Ly6)/Plaur domain-containing 1 (Lypd1), was specifically expressed in preodontoblasts. Depletion of Lypd1 in tooth germ using an ex vivo organ culture system and in mouse dental pulp (mDP) cells resulted in the inhibition of odontoblast differentiation. Activation of bone morphogenetic protein (BMP) signaling by BMP2 treatment in mDP cells promoted odontoblast differentiation via phosphorylation of Smad1/5/8, while this BMP2-mediated odontoblast differentiation was inhibited by depletion of Lypd1. Furthermore, we created a deletion construct of the C-terminus containing the omega site in LYPD1; this site is necessary for localizing GPI-APs to the plasma membrane and lipid rafts. We identified that this site is essential for odontoblast differentiation and morphological change of mDP cells. These findings demonstrated that LYPD1 is a novel marker of preodontoblasts in the developing tooth; additionally, they suggest that LYPD1 is important for tooth development and that it plays a pivotal role in odontoblast differentiation by regulating Smad1/5/8 phosphorylation through its effect as a GPI-AP in lipid rafts.

  18. Single-cell RNA-sequence of dental epithelium reveals responsible genes of dental anomalies in human Peer-reviewed

    Kifu Miyata, Yuta Chiba, Triana Marchelina, Saori Inada, Sae Oka, Kan Saito, Aya Yamada, Satoshi Fukumoto

    Pediatric Dental Journal　2023/03

    Publisher: Elsevier BV

    DOI： 10.1016/j.pdj.2023.03.004 　

    ISSN： 0917-2394

  19. Development of a novel ex vivo organ culture system to improve preservation methods of regenerative tissues. International-journal Peer-reviewed

    Tomomi Yuta, Tian Tian, Yuta Chiba, Kanako Miyazaki, Keita Funada, Kanji Mizuta, Yao Fu, Jumpei Kawahara, Tsutomu Iwamoto, Ichiro Takahashi, Satoshi Fukumoto, Keigo Yoshizaki

    Scientific reports　13　(1)　3354-3354　2023/02/27

    DOI： 10.1038/s41598-023-29629-2 　

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    Recent advances in regenerative technology have made the regeneration of various organs using pluripotent stem cells possible. However, a simpler screening method for evaluating regenerated organs is required to apply this technology to clinical regenerative medicine in the future. We have developed a simple evaluation method using a mouse tooth germ culture model of organs formed by epithelial-mesenchymal interactions. In this study, we successfully established a simple method that controls tissue development in a temperature-dependent manner using a mouse tooth germ ex vivo culture model. We observed that the development of the cultured tooth germ could be delayed by low-temperature culture and resumed by the subsequent culture at 37 °C. Furthermore, the optimal temperature for the long-term preservation of tooth germ was 25 °C, a subnormothermic temperature that maintains the expression of stem cell markers. We also found that subnormothermic temperature induces the expression of cold shock proteins, such as cold-inducible RNA-binding protein, RNA-binding motif protein 3, and serine and arginine rich splicing factor 5. This study provides a simple screening method to help establish the development of regenerative tissue technology using a tooth organ culture model. Our findings may be potentially useful for making advances in the field of regenerative medicine.

  20. Japanese Laws and the Current Status of Regenerative Medicine in the Tohoku Region. (review) International-journal Peer-reviewed

    Yuya Kamano, Noboru Terajima, Yuta Chiba, Venkata V Suresh, Masahiro Saito

    The journal of contemporary dental practice　24　(2)　120-128　2023/02/01

    DOI： 10.5005/jp-journals-10024-3487 　

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    AIM: The aim of this study was to review Japanese laws regarding regenerative medicine and the current status of clinical application of regenerative medicine, to learn about the advantages and problems, and to thereby serve as a reference for measures necessary for the development of regenerative medicine. BACKGROUND: Regenerative medicine started in 1957 with the transplantation of hematopoietic stem cells, followed by the establishment of embryonic stem cells in 1981 and induced pluripotent stem cells in 2006, and continues to evolve progressively. At the same time, however, problems have emerged due to lax legal regulations, such as the use of treatments that lack scientific evidence. REVIEW RESULTS: The Japanese government enacted two laws to regulate regenerative medicine: the Law to Ensure the Safety of Regenerative Medicine and the Amend the Pharmaceutical Affairs Law in 2013. These laws were enacted with the aim of providing safe regenerative medicine promptly and smoothly and developing many regenerative medicine products. In these laws, regenerative medicine is defined as medical treatment that restores lost functions of damaged organs and tissues with the help of cellular and tissue-based products. Nowadays, there are two major methods of regenerative medicine. One representative method involves the transplantation of devices that activates self-regenerative ability by introducing living cells into patients' body. The other method is the activation and differentiation of endogenous stem cells with cell growth and differentiation factors. CONCLUSION: The current status of regenerative medicine in the Tohoku region after the enactment of these laws is described in detail. This clarified the advantages and disadvantages associated with regenerative medicine as it is currently practiced in Japan. CLINICAL SIGNIFICANCE: Development of regenerative medicine in dentistry will be advanced by learning about its clinical application in medicine.

  21. GSK3beta inhibitor-induced dental mesenchymal stem cells regulate ameloblast differentiation. International-journal Peer-reviewed

    Aya Yamada, Keigo Yoshizaki, Kan Saito, Masaki Ishikawa, Yuta Chiba, Seira Hoshikawa, Mitsuki Chiba, Ryoko Hino, Yuriko Maruya, Hiroshi Sato, Keiji Masuda, Haruyoshi Yamaza, Takashi Nakamura, Tsutomu Iwamoto, Satoshi Fukumoto

    Journal of oral biosciences　64　(4)　400-409　2022/10/18

    DOI： 10.1016/j.job.2022.10.002 　

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    OBJECTIVES: Epithelial-mesenchymal interactions are extremely important in tooth development and essential for ameloblast differentiation, especially during tooth formation. We aimed to identify the type of mesenchymal cells important in ameloblast differentiation. METHODS: We used two types of cell culture systems with chambers and found that a subset of dental mesenchymal cells is important for the differentiation of dental epithelial cells into ameloblasts. Among odontogenic mesenchymal cells, dental pulp stem cell-like cells induced the expression of ameloblast differentiation markers. Therefore, we induced dental pulp stem cell-like cells from dental pulp stem cells using the small molecule compound BIO (a GSK-3 inhibitor IX) to clarify the mechanism involved in inducing ameloblast differentiation of dental pulp stem cells. RESULTS: The BIO-induced dental pulp cells promoted the expression of mesenchymal stem cell markers Oct3/4 and Bcrp1. Furthermore, we used artificial dental pulp stem cells induced by BIO to identify the molecules expressed in dental pulp stem cells required for ameloblast differentiation. Panx3 expression was induced in the dental pulp stem cell through interaction with the dental epithelial cells. In addition, ATP release from cells increased in Panx3-expressing cells. We also confirmed that ATP stimulation is accepted in dental epithelial cells. CONCLUSIONS: These results showed that the Panx3 expressed in dental pulp stem cells is important for ameloblast differentiation and that ATP release by Panx3 may play a role in epithelial-mesenchymal interaction.

  22. Enamel defects of Axenfeld-Rieger syndrome and the role of PITX2 in its pathogenesis. International-journal Peer-reviewed

    Yi Yang, Junxia Zhu, Yuta Chiba, Satoshi Fukumoto, Man Qin, Xin Wang

    Oral diseases　2022/07/14

    DOI： 10.1111/odi.14315 　

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    OBJECTIVES: To investigate the detailed ultrastructural patterns of dental abnormalities affected by Axenfeld-Rieger syndrome (ARS) with a heterozygous microdeletion involving paired-like homeodomain 2 (PITX2) and explored the underlying molecular mechanisms driving enamel defects. SUBJECTS AND METHODS: Sanger sequencing, genomic quantitative PCR analysis, and chromosomal microarray analysis were used to screen the disease-causing mutation in one ARS proband. An exfoliated tooth from an ARS patient was analyzed with scanning electron microscopy and micro-computerized tomography. A stable Pitx2 knockdown cell line was generated to simulate PITX2 haploinsufficiency. Cell proliferation and ameloblast differentiation were analyzed, and the role of the Wnt/β-catenin pathway in proliferation of ameloblast precursor cells was investigated. RESULTS: An approximately 0.216 Mb novel deletion encompassing PITX2 was identified. The affected tooth displayed a thinner and broken layer of enamel and abnormal enamel biomineralization. PITX2 downregulation inhibited the proliferation and differentiation of inner enamel epithelial cells, and LiCl stimulation partially reversed the proliferation ability after Pitx2 knockdown. CONCLUSIONS: Enamel formation is disturbed in some patients with ARS. Pitx2 knockdown can influence the proliferation and ameloblast differentiation of inner enamel epithelial cells, and PITX2 may regulate cell proliferation via Wnt/β-catenin signaling pathway.

  23. An ex vivo organ culture screening model revealed that low temperature conditions prevent side effects of anticancer drugs. International-journal Peer-reviewed

    Tian Tian, Kanako Miyazaki, Yuta Chiba, Keita Funada, Tomomi Yuta, Kanji Mizuta, Yao Fu, Jumpei Kawahara, Xue Han, Yuna Ando, Ami Funada, Aya Yamada, Tsutomu Iwamoto, Seiji Nakamura, Ichiro Takahashi, Satoshi Fukumoto, Keigo Yoshizaki

    Scientific reports　12　(1)　3093-3093　2022/02/23

    DOI： 10.1038/s41598-022-06945-7 　

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    Development of chemotherapy has led to a high survival rate of cancer patients; however, the severe side effects of anticancer drugs, including organ hypoplasia, persist. To assume the side effect of anticancer drugs, we established a new ex vivo screening model and described a method for suppressing side effects. Cyclophosphamide (CPA) is a commonly used anticancer drug and causes severe side effects in developing organs with intensive proliferation, including the teeth and hair. Using the organ culture model, we found that treatment with CPA disturbed the growth of tooth germs by inducing DNA damage, apoptosis and suppressing cellular proliferation and differentiation. Furthermore, low temperature suppressed CPA-mediated inhibition of organ development. Our ex vivo and in vitro analysis revealed that low temperature impeded Rb phosphorylation and caused cell cycle arrest at the G1 phase during CPA treatment. This can prevent the CPA-mediated cell damage of DNA replication caused by the cross-linking reaction of CPA. Our findings suggest that the side effects of anticancer drugs on organ development can be avoided by maintaining the internal environment under low temperature.

  24. シングルセルRNAシーケンスによる歯原性細胞マーカー遺伝子の探索と機能解析 (review) Invited

    千葉 雄太

    小児歯科学雑誌　60　(1)　1-7　2022/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  25. The tooth-specific basic helix-loop-helix factor AmeloD promotes differentiation of ameloblasts. International-journal Peer-reviewed

    LingLing Jia, Yuta Chiba, Kan Saito, Keigo Yoshizaki, Tian Tian, Xu Han, Kanji Mizuta, Mitsuki Chiba, Xin Wang, Shahad Al Thamin, Aya Yamada, Satoshi Fukumoto

    Journal of cellular physiology　237　(2)　1597-1606　2021/11/23

    DOI： 10.1002/jcp.30639 　

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    Tissue-specific basic helix-loop-helix (bHLH) transcription factors play an important role in cellular differentiation. We recently identified AmeloD as a tooth-specific bHLH transcription factor. However, the role of AmeloD in cellular differentiation has not been investigated. The aim of this study was to elucidate the role of AmeloD in dental epithelial cell differentiation. We found that AmeloD-knockout (AmeloD-KO) mice developed an abnormal structure and altered ion composition of enamel in molars, suggesting that AmeloD-KO mice developed enamel hypoplasia. In molars of AmeloD-KO mice, the transcription factor Sox21 encoding SRY-Box transcription factor 21 and ameloblast differentiation marker genes were significantly downregulated. Furthermore, overexpression of AmeloD in the dental epithelial cell line M3H1 upregulated Sox21 and ameloblast differentiation marker genes, indicating that AmeloD is critical for ameloblast differentiation. Our study demonstrated that AmeloD is an important transcription factor in amelogenesis for promoting ameloblast differentiation. This study provides new insights into the mechanisms of amelogenesis.

  26. Integration of Single-Cell RNA- and CAGE-seq Reveals Tooth-Enriched Genes. International-journal Peer-reviewed

    Y Chiba, K Yoshizaki, T Tian, K Miyazaki, D Martin, K Saito, A Yamada, S Fukumoto

    Journal of dental research　220345211049785-220345211049785　2021/11/20

    DOI： 10.1177/00220345211049785 　

    More details Close

    Organ development is dictated by the regulation of genes preferentially expressed in tissues or cell types. Gene expression profiling and identification of specific genes in organs can provide insights into organogenesis. Therefore, genome-wide analysis is a powerful tool for clarifying the mechanisms of development during organogenesis as well as tooth development. Single-cell RNA sequencing (scRNA-seq) is a suitable tool for unraveling the gene expression profile of dental cells. Using scRNA-seq, we can obtain a large pool of information on gene expression; however, identification of functional genes, which are key molecules for tooth development, via this approach remains challenging. In the present study, we performed cap analysis of gene expression sequence (CAGE-seq) using mouse tooth germ to identify the genes preferentially expressed in teeth. The CAGE-seq counts short reads at the 5'-end of transcripts; therefore, this method can quantify the amount of transcripts without bias related to the transcript length. We hypothesized that this CAGE data set would be of great help for further understanding a gene expression profile through scRNA-seq. We aimed to identify the important genes involved in tooth development via bioinformatics analyses, using a combination of scRNA-seq and CAGE-seq. We obtained the scRNA-seq data set of 12,212 cells from postnatal day 1 mouse molars and the CAGE-seq data set from postnatal day 1 molars. scRNA-seq analysis revealed the spatiotemporal expression of cell type-specific genes, and CAGE-seq helped determine whether these genes are preferentially expressed in tooth or ubiquitously. Furthermore, we identified candidate genes as novel tooth-enriched and dental cell type-specific markers. Our results show that the integration of scRNA-seq and CAGE-seq highlights the genes important for tooth development among numerous gene expression profiles. These findings should contribute to resolving the mechanism of tooth development and establishing the basis for tooth regeneration in the future.

  27. Sp6/Epiprofin is a master regulator in the developing tooth Peer-reviewed

    Craig S. Rhodes, Yasuo Yoshitomi, Peter D. Burbelo, Nowlan H. Freese, Takashi Nakamura, Yuta Chiba, Yoshihiko Yamada

    Biochemical and Biophysical Research Communications　581　89-95　2021/10

    Publisher: Elsevier {BV}

    DOI： 10.1016/j.bbrc.2021.10.017 　

    ISSN： 0006-291X

    eISSN： 1090-2104

  28. Connexin 43-Mediated Gap Junction Communication Regulates Ameloblast Differentiation via ERK1/2 Phosphorylation. International-journal Peer-reviewed

    Aya Yamada, Keigo Yoshizaki, Masaki Ishikawa, Kan Saito, Yuta Chiba, Emiko Fukumoto, Ryoko Hino, Seira Hoshikawa, Mitsuki Chiba, Takashi Nakamura, Tsutomu Iwamoto, Satoshi Fukumoto

    Frontiers in physiology　12　748574-748574　2021/09

    DOI： 10.3389/fphys.2021.748574 　

    More details Close

    Connexin 43 (Cx43) is an integral membrane protein that forms gap junction channels. These channels mediate intercellular transport and intracellular signaling to regulate organogenesis. The human disease oculodentodigital dysplasia (ODDD) is caused by mutations in Cx43 and is characterized by skeletal, ocular, and dental abnormalities including amelogenesis imperfecta. To clarify the role of Cx43 in amelogenesis, we examined the expression and function of Cx43 in tooth development. Single-cell RNA-seq analysis and immunostaining showed that Cx43 is highly expressed in pre-secretory ameloblasts, differentiated ameloblasts, and odontoblasts. Further, we investigated the pathogenic mechanisms of ODDD by analyzing Cx43-null mice. These mice developed abnormal teeth with multiple dental epithelium layers. The expression of enamel matrix proteins such as ameloblastin (Ambn), which is critical for enamel formation, was significantly reduced in Cx43-null mice. TGF-β1 induces Ambn transcription in dental epithelial cells. The induction of Ambn expression by TGF-β1 depends on the density of the cultured cells. Cell culture at low densities reduces cell-cell contact and reduces the effect of TGF-β1 on Ambn induction. When cell density was high, Ambn expression by TGF-β1 was enhanced. This induction was inhibited by the gap junction inhibitors, oleamide, and 18α-grycyrrhizic acid and was also inhibited in cells expressing Cx43 mutations (R76S and R202H). TGF-β1-mediated phosphorylation and nuclear translocation of ERK1/2, but not Smad2/3, were suppressed by gap junction inhibitors. Cx43 gap junction activity is required for TGF-β1-mediated Runx2 phosphorylation through ERK1/2, which forms complexes with Smad2/3. In addition to its gap junction activity, Cx43 may also function as a Ca2+ channel that regulates slow Ca2+ influx and ERK1/2 phosphorylation. TGF-β1 transiently increases intracellular calcium levels, and the increase in intracellular calcium over a short period was not related to the expression level of Cx43. However, long-term intracellular calcium elevation was enhanced in cells overexpressing Cx43. Our results suggest that Cx43 regulates intercellular communication through gap junction activity by modulating TGF-β1-mediated ERK signaling and enamel formation.

  29. Transcriptional regulation of the basic helix‐loop‐helix factor AmeloD during tooth development International-journal Peer-reviewed

    Shahad Al Thamin, Yuta Chiba, Keigo Yoshizaki, Tian Tian, LingLing Jia, Xin Wang, Kan Saito, Jiyao Li, Aya Yamada, Satoshi Fukumoto

    Journal of Cellular Physiology　2021/04/12

    Publisher: Wiley

    DOI： 10.1002/jcp.30389 　

    More details Close

    The epithelial-mesenchymal interactions are essential for the initiation and regulation of the development of teeth. Following the initiation of tooth development, numerous growth factors are secreted by the dental epithelium and mesenchyme that play critical roles in cellular differentiation. During tooth morphogenesis, the dental epithelial stem cells differentiate into several cell types, including inner enamel epithelial cells, which then differentiate into enamel matrix-secreting ameloblasts. Recently, we reported that the novel basic-helix-loop-helix transcription factor, AmeloD, is actively engaged in the development of teeth as a regulator of dental epithelial cell motility. However, the gene regulation mechanism of AmeloD is still unknown. In this study, we aimed to uncover the mechanisms regulating AmeloD expression during tooth development. By screening growth factors that are important in the early stages of tooth formation, we found that TGF-β1 induced AmeloD expression and ameloblast differentiation in the dental epithelial cell line, SF2. TGF-β1 phosphorylated ERK1/2 and Smad2/3 to induce AmeloD expression, whereas treatment with the MEK inhibitor, U0126, inhibited AmeloD induction. Promoter analysis of AmeloD revealed that the proximal promoter of AmeloD showed high activity in dental epithelial cell lines, which was enhanced following TGF-β1 stimulation. These results suggested that TGF-β1 activates AmeloD transcription via ERK1/2 phosphorylation. Our findings provide new insights into the mechanisms that govern tooth development.

  30. Melnick-Needles syndrome associated molecule, Filamin-A regulates dental epithelial cell migration and root formation Peer-reviewed

    Ryoko Hino, Aya Yamada, Yuta Chiba, Keigo Yoshizaki, Emiko Fukumoto, Tsutomu Iwamoto, Yuriko Maruya, Keishi Otsu, Hidemistu Harada, Kan Saito, Satoshi Fukumoto

    Pediatric Dental Journal　30　(3)　208-214　2020/12

    DOI： 10.1016/j.pdj.2020.09.003 　

    ISSN： 0917-2394

    eISSN： 1880-3997

  31. G protein-coupled receptor Gpr115 (Adgrf4) is required for enamel mineralization mediated by ameloblasts International-journal Peer-reviewed

    Yuta Chiba, Keigo Yoshizaki, Kan Saito, Tomoko Ikeuchi, Tsutomu Iwamoto, Craig Rhodes, Takashi Nakamura, Susana de Vega, Robert J. Morell, Erich T. Boger, Daniel Martin, Ryoko Hino, Hiroyuki Inuzuka, Christopher K.E. Bleck, Aya Yamada, Yoshihiko Yamada, Satoshi Fukumoto

    Journal of Biological Chemistry　295　(45)　15328-15341　2020/11/06

    DOI： 10.1074/jbc.RA120.014281 　

    ISSN： 0021-9258

    eISSN： 1083-351X

  32. Expression Patterns of Claudin Family Members During Tooth Development and the Role of Claudin-10 (Cldn10) in Cytodifferentiation of Stratum Intermedium Peer-reviewed

    Xin Wang, Yuta Chiba, Lingling Jia, Keigo Yoshizaki, Kan Saito, Aya Yamada, Man Qin, Satoshi Fukumoto

    Frontiers in Cell and Developmental Biology　8　2020/10/22

    Publisher: Frontiers Media {SA}

    DOI： 10.3389/fcell.2020.595593 　

    ISSN： 2296-634X

    eISSN： 2296-634X

  33. Single-Cell RNA-Sequencing From Mouse Incisor Reveals Dental Epithelial Cell-Type Specific Genes Peer-reviewed

    Yuta Chiba, Kan Saito, Daniel Martin, Erich T. Boger, Craig Rhodes, Keigo Yoshizaki, Takashi Nakamura, Aya Yamada, Robert J. Morell, Yoshihiko Yamada, Satoshi Fukumoto

    Frontiers in Cell and Developmental Biology　8　2020/09/01

    DOI： 10.3389/fcell.2020.00841 　

    ISSN： 2296-634X

    eISSN： 2296-634X

  34. Sox21 Regulates Anapc10 Expression and Determines the Fate of Ectodermal Organ Peer-reviewed

    Kan Saito, Frederic Michon, Aya Yamada, Hiroyuki Inuzuka, Satoko Yamaguchi, Emiko Fukumoto, Keigo Yoshizaki, Takashi Nakamura, Makiko Arakaki, Yuta Chiba, Masaki Ishikawa, Hideyuki Okano, Irma Thesleff, Satoshi Fukumoto

    iScience　23　(7)　101329-101329　2020/07/24

    Publisher: Elsevier BV

    DOI： 10.1016/j.isci.2020.101329 　

    ISSN： 2589-0042

    eISSN： 2589-0042

  35. Identification and function analysis of ameloblast differentiation-related molecules using mouse incisors Invited

    Saito Kan, Chiba Yuta, Yamada Aya, Fukumoto Satoshi

    Pediatric Dental Journal　30　(3)　2020

    ISSN： 0917-2394

  36. Perlecan regulates pericyte dynamics in the maintenance and repair of the blood-brain barrier International-journal Peer-reviewed

    Kuniyuki Nakamura, Tomoko Ikeuchi, Kazuki Nara, Craig S. Rhodes, Peipei Zhang, Yuta Chiba, Saiko Kazuno, Yoshiki Miura, Tetsuro Ago, Eri Arikawa-Hirasawa, Yoh Suke Mukouyama, Yoshihiko Yamada

    Journal of Cell Biology　218　(10)　3506-3525　2019/10/07

    DOI： 10.1083/JCB.201807178 　

    ISSN： 0021-9525

    eISSN： 1540-8140

  37. Pannexin-3 Deficiency Delays Skin Wound Healing in Mice due to Defects in Channel Functionality Peer-reviewed

    Peipei Zhang, Masaki Ishikawa, Craig Rhodes, Andrew Doyle, Tomoko Ikeuchi, Kuniyuki Nakamura, Yuta Chiba, Bing He, Yoshihiko Yamada

    Journal of Investigative Dermatology　139　(4)　909-918　2019/04

    DOI： 10.1016/j.jid.2018.08.033 　

    ISSN： 0022-202X

    eISSN： 1523-1747

  38. The transcription factor AmeloD stimulates epithelial cell motility essential for tooth morphology Peer-reviewed

    Chiba Y, He B, Yoshizaki K, Rhodes C, Ishijima M, Bleck CKE, Stempinski E, Chu EY, Nakamura T, Iwamoto T, de Vega S, Saito K, Fukumoto S, Yamada Y.

    Journal of Biological Chemistry　Vol.294　(No.10)　3406-3418　2019/03/08

    DOI： 10.1074/jbc.ra118.005298 　

    ISSN： 0021-9258 1083-351X

    More details Close

    The development of ectodermal organs, such as teeth, requires epithelial-mesenchymal interactions. Basic-helix-loop-helix (bHLH) transcription factors regulate various aspects of tissue development, and we have previously identified a bHLH transcription factor, AmeloD, from a tooth germ cDNA library. Here, we provide both in vitro and in vivo evidence that AmeloD is important in tooth development. We created AmeloD knockout (KO) mice to identify the in vivo functions of AmeloD that are critical for tooth morphogenesis. We found that AmeloD KO mice developed enamel hypoplasia and small teeth because of increased expression of E-cadherin in inner enamel epithelial (IEE) cells and it may cause inhibition of the cellmigration. We used the CLDE dental epithelial cell line to conduct further mechanistic analyses to determine if AmeloD overexpression in CLDE cells suppresses E-cadherin expression and promotes cell migration. Knockout of epiprofin (Epfn), another transcription factor required for tooth morphogenesis and development, and analysis of AmeloD expression and deletion revealed that AmeloD also contributed to multiple tooth formation in Epfn KO mice by promoting the invasion of dental epithelial cells into the mesenchymal region. Thus, AmeloD appears to play an important role in tooth morphogenesis by modulating E-cadherin and dental epithelial-mesenchymal interactions. These findings provide detailed insights into the mechanism of ectodermal organ development.

  39. The transcription factor NKX2-3 mediates p21 expression and ectodysplasin-A signaling in the enamel knot for cusp formation in tooth development Peer-reviewed

    Han X, Yoshizaki K, Miyazaki K, Arai C, Funada K, Yuta T, Tian T, Chiba Y, Saito K, Iwamoto T, Yamada A, Takahashi I, Fukumoto S.

    Journal of Biological Chemistry　Vol.293　(No.38)　14572-14584　2018/09/21

    DOI： 10.1074/jbc.ra118.003373 　

    ISSN： 0021-9258 1083-351X

    More details Close

    Tooth morphogenesis is initiated by reciprocal interactions between the ectoderm and neural crest-derived mesenchyme. During tooth development, tooth cusps are regulated by precise control of proliferation of cell clusters, termed enamel knots, that are present among dental epithelial cells. The interaction of ectodysplasin-A (EDA) with its receptor, EDAR, plays a critical role in cusp formation by these enamel knots, and mutations of these genes is a cause of ectodermal dysplasia. It has also been reported that deficiency in , encoding a member of the NK2 homeobox family of transcription factors, leads to cusp absence in affected teeth. However, the molecular role of NKX2-3 in tooth morphogenesis is not clearly understood. Using gene microarray analysis in mouse embryos, we found that is highly expressed during tooth development and increased during the tooth morphogenesis, especially during cusp formation. We also demonstrate that NKX2-3 is a target molecule of EDA and critical for expression of the cell cycle regulator p21 in the enamel knot. Moreover, NKX2-3 activated the bone morphogenetic protein (BMP) signaling pathway by up-regulating expression levels of and in dental epithelium and decreased the expression of the dental epithelial stem cell marker SRY box 2 (SOX2). Together, our results indicate that EDA/NKX2-3 signaling is essential for enamel knot formation during tooth morphogenesis in mice.

  40. Material properties on enamel and fissure of surface pre-reacted glass-ionomer filler-containing dental sealant Peer-reviewed

    Koji Hirayama, Takashi Hanada, Ryoko Hino, Kan Saito, Mayu Kobayashi, Makiko Arakaki, Yuta Chiba, Norihiko Nakamura, Takeshi Sakurai, Tsutomu Iwamoto, Satoshi Fukumoto, Aya Yamada

    Pediatric Dental Journal　28　(2)　87-95　2018/08

    DOI： 10.1016/j.pdj.2018.05.001 　

    ISSN： 0917-2394

    eISSN： 1880-3997

  41. Identification of the Novel Dental Epithelium-Specific Transcription Factor AmeloD. Peer-reviewed

    Bing He, Yuta Chiba, Haochuan Li, Susana de Vega, Kazuhiro Tanaka, Keigo Yoshizaki, Muneaki Ishijima, Kenji Yuasa, Masaki Ishikawa, Craig Rhodes, Kiyoshi Sakai, Peipei Zhang, Satoshi Fukumoto, Xuedong Zhou, Yoshihiko Yamada

    J Dent Res.　2018/01

  42. Globoside accelerates the differentiation of dental epithelial cells into ameloblasts Peer-reviewed

    Takashi Nakamura, Yuta Chiba, Masahiro Naruse, Kan Saito, Hidemitsu Harada, Satoshi Fukumoto

    International Journal of Oral Science　8　(4)　205-212　2016/12/16

    DOI： 10.1038/ijos.2016.35 　

    ISSN： 1674-2818

    eISSN： 2049-3169

  43. Novel hedgehog agonists promote osteoblast differentiation in mesenchymal stem cells Peer-reviewed

    Takashi Nakamura, Masahiro Naruse, Yuta Chiba, Toshihisa Komori, Keiichi Sasaki, Masahiro Iwamoto, Satoshi Fukumoto

    Journal of Cellular Physiology　230　(4)　922-929　2015/04

    DOI： 10.1002/jcp.24823 　

    ISSN： 0021-9541

    eISSN： 1097-4652

  44. Evaluation of the optimal exposure settings for occlusal photography with digital cameras Peer-reviewed

    Yu Sugawara, Kan Saito, Masaharu Futaki, Masahiro Naruse, Mariko Ono, Ryoko Hino, Yuta Chiba, Makiko Arakaki, Aya Yamada, Satoshi Fukumoto

    Pediatric Dental Journal　24　(2)　89-96　2014/01

    Publisher: Elsevier Ltd

    DOI： 10.1016/j.pdj.2014.04.002 　

    ISSN： 0917-2394

    eISSN： 1880-3997

Show all ︎Show first 5

Misc. 72

  1. Plod2 regulates ameloblast differentiation and cell proliferation

    Wanshu Li, Yuta Chiba, Kan Saito, Takashi Nakamura, Satoshi Fukumoto

    第87回東北大学歯学会　2026/06

  2. Comprehensive analyses of desmosome family members during tooth development and the role of Desmocollin-3 (Dsc3) in cytodifferentiation of stratum intermedium

    Triana Marchelina, Yuta Chiba, Shinji Otake, Li Wanshu, Aya Yamada, Satoshi Fukumoto, Kan Saito

    第64回日本小児歯科学会学術大会　2026/05

  3. Plod2 as a Novel Marker Gene of Pre-ameloblast Differentiation

    Wanshu Li, Yuta Chiba, Triana Marchelina, Shinji Otake, Mitsuki Chiba, Aya Yamada, Satoshi Fukumoto

    104th General Session & Exhibition of the IADR　2026/03

  4. 臨床・再生医学から見た歯科基礎医学の新たな可能性 臨床疾患から見た歯の発生と再生

    福本 敏, 千葉 雄太, 吉崎 恵悟

    Journal of Oral Biosciences Supplement　2025　11-11　2025/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  5. AmeloD binds to TCF4 during tooth formation

    Airi Ishikawa, Hiroshi Sato, Sae Oka, Yuta Chiba, Aya Yamada, Satoshi Fukumoto

    The 34th Annual Congress of Taiwan Academy of Pediatric Dentistry (TAPD 2025)　2025/06

  6. The role of tooth specific transcription factor AmeloD in ameloblast differentiation

    Chinatsu Misago, Hiroshi Sato, Akane Shimada, Sae Oka, Itaru Komine, Atsuhide Sasaki, Yuta Chiba, Aya Yamada, Satoshi Fukumoto

    The 66th Korean Academy of Pediatric Dentistry 2025 Conference　2025/04

  7. Phenotypic analysis of dental pulp stem cells derived from deciduous teeth in Down syndrome

    Itaru Komine, Yuta Chiba, Hiroshi Sato, Sae Oka, Keigo Yoshizaki, Aya Yamada, Satoshi Fukumoto

    The 66th Korean Academy of Pediatric Dentistry 2025 Conference　2025/04

  8. 新規合着用セメントが象牙質脱灰に及ぼす影響

    大竹 慎司, 日野 綾子, ただ野 愛実, 千葉 雄太, 中村 友昭, 丸谷 由里子, 齋藤 幹

    小児歯科学雑誌　63　(地方会抄録号)　3-3　2025/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  9. 新規知覚過敏抑制材における抗脱灰作用の評価

    Yun Tsai, 大竹 慎司, ただ野 愛実, 千葉 雄太, 日野 綾子, 中村 友昭, 丸谷 由里子, 齋藤 幹

    小児歯科学雑誌　63　(地方会抄録号)　3-4　2025/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  10. Regional odontodysplasiaの口腔管理の2例

    中村 友昭, 大竹 慎司, 丸谷 由里子, 日野 綾子, 千葉 雄太, ただ野 愛実, 齋藤 幹, 笠原 一規

    小児歯科学雑誌　63　(地方会抄録号)　7-7　2025/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  11. 歯原性間葉組織に特異的に発現する遺伝子の小児慢性特定疾病との関連について

    庄 璃音, 千葉 雄太, 小窪 秀義, 千葉 満生, 佐藤 浩, 廣藤 雄太, 高山 扶美子, 山田 亜矢, 福本 敏

    小児歯科学雑誌　63　(地方会抄録号)　84-84　2025/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  12. Expression analysis of AmeloD as a novel biomarker gene of ameloblastoma

    千葉雄太, 大竹慎司, 有川聖良, 山田亜矢, 齋藤幹, 福本敏

    小児歯科学雑誌　63　(大会抄録号)　140-140　2025

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  13. Role of AmeloD and ODAM in Enamel Formation

    Sae Oka, Hiroshi Sato, Yuta Chiba, Saori Inada, Akane Shimada, Matsuri Takahashi, Aya Yamada, Satoshi Fukumoto

    The 13th Pediatric Dentistry Association of Asia 2024　2024/11

  14. Profiling desmosome-related genes that associated to dental anomalies using single cell RNA-sequence

    Marchelina Triana, Yuta Chiba, Shinji Otake, Mitsuki Chiba, Kan Saito, Aya Yamada, Satoshi Fukumoto

    The 13th Pediatric Dentistry Association of Asia 2024　2024/11

  15. The crucial role of Keratin 15 in tooth morphogenesis revealed by single-cell RNA sequencing of tooth germ

    Yuta Chiba, Saori Inada, Sae Oka, Akane Shimada, Kan Saito, Aya Yamada, Satoshi Fukumoto

    The 13th Pediatric Dentistry Association of Asia 2024　2024/11

  16. Single-cell RNA-sequence reveals distribution of cytokeratin family in dental epithelial cell types

    Saori Inada, Yuta Chiba, Hiroshi Sato, Sae Oka, Keigo Yoshizaki, Aya Yamada, Satoshi Fukumoto

    The 65th Korean Academy of Pediatric Dentistry 2024 Conference　2024/04

  17. シングルセルRNAシークエンスを基盤とした歯の発生機構解明と疾患機序探索への応用

    千葉雄太

    小児歯科学雑誌　62　2024

    ISSN： 0583-1199

  18. Identification of pre-ameloblast marker genes using single-cell RNA-sequence

    LI Wanshu, 千葉雄太, 千葉満生, MARCHELINA Triana, 大竹慎司, 齋藤幹, 山田亜矢, 福本敏, 福本敏

    小児歯科学雑誌　62　2024

    ISSN： 0583-1199

  19. Effect of S100a6 on differentiation of dental epithelial cells

    大竹慎司, 齋藤幹, 千葉雄太, 山田亜矢, 福本敏, 福本敏

    小児歯科学雑誌　62　2024

    ISSN： 0583-1199

  20. 歯胚のシングルセルRNAシークエンスを応用した疾患関連遺伝子の同定と歯の発生過程における発現解析

    Triana Marchelina, 千葉雄太, 齋藤 幹, 山田亜矢, 福本 敏

    第41回日本小児歯科学会北日本地方会　62　2023/10

    ISSN： 0583-1199

  21. S100a6によるエナメル芽細胞の増殖と分化への影響

    大竹 慎司, 齋藤 幹, 千葉 雄太, 山田 亜矢, 福本 敏

    第65回歯科基礎医学会学術大会　2023　[P2-21]　2023/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  22. S100a6はエナメル芽細胞の分化を調節する

    大竹 慎司, 齋藤 幹, 千葉 雄太, 吉岡 直哉, 室月 研, 山田 亜矢, 福本 敏

    東北大学歯学雑誌　41/42　(2/1)　45-45　2023/06

    Publisher: 東北大学歯学会

    ISSN： 0287-3915

  23. Tooth specific molecule amelod interacted with ODAM during amelogenesis

    S. Oka, H. Sato, Y. Chiba, S. Inada, A. Yamada, S. Fukumoto

    the 29th Congress of the International Association of Paediatric Dentistry　2023/06

  24. シングルセル解析を用いた象牙質形成不全症関連遺伝子の同定

    宮田 貴楓, 千葉 雄太, 齋藤 幹, 山田 亜矢, 福本 敏

    小児歯科学雑誌　61　(地方会抄録号)　11-11　2023/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  25. 混合型脈管奇形の患児の口腔管理の1例

    木舩 崇, 山座 治義, 増田 啓次, 小笠原 貴子, 高山 扶美子, 千葉 雄太, 廣藤 雄太, 佐藤 綾子, 福本 敏

    小児歯科学雑誌　61　(地方会抄録号)　75-75　2023/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  26. 外傷により完全陥入した上顎乳側切歯が抜歯に至った1例

    佐藤 綾子, 高山 扶美子, 小笠原 貴子, 山座 治義, 増田 啓次, 廣藤 雄太, 千葉 雄太, 木舩 崇, 伊藤 洋介, 田中 絢子, 稲田 幸織, 福本 敏

    小児歯科学雑誌　61　(地方会抄録号)　76-77　2023/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  27. シングルセルRNAシークエンスを用いた歯に異常をきたす遺伝性疾患の同定

    宮田 貴楓, 千葉 雄太, 斎藤 幹, 山田 亜矢, 福本 敏

    小児歯科学雑誌　61　(地方会抄録号)　82-82　2023/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  28. パーキンソン病病態と関連した破骨細胞分化を促進する新たな脱ユビキチン化経路の同定(Deubiquitinase-mediated regulation of osteoclast differentiation)

    千葉 満生, 星川 聖良, 齋藤 幹, 千葉 雄太, 山田 亜矢, 福本 敏

    Journal of Oral Biosciences Supplement　2022　180-180　2022/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  29. GPIアンカー型タンパク質Lypd1は、前象牙芽細胞特異的に発現し象牙芽細胞分化を制御する(GPI-anchored protein Lypd1 is specifically expressed on preodontoblast and regulates odontoblast differentiation)

    傅 堯, 宮崎 佳奈子, 吉崎 恵悟, 千葉 雄太, 川原 純平, 湯田 智美, 田 甜, 水田 敢士, 福本 敏, 高橋 一郎

    Journal of Oral Biosciences Supplement　2022　237-237　2022/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  30. 歯特異的転写因子AmeloD結合タンパク質の酵母Two-Hybrid法によるスクリーニング(Screening of proteins binding to tooth specific transcription factor AmeloD by yeast two-hybrid system)

    岡 桜恵, 佐藤 浩, 千葉 雄太, 吉崎 恵悟, 福本 敏

    Journal of Oral Biosciences Supplement　2022　244-244　2022/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  31. 口腔科学から発信する再生医療のSDGsと未来 シングルセルRNAシークエンスを用いた歯の発生基盤の解明と再生医療への応用

    千葉 雄太, 福本 敏

    日本口腔科学会雑誌　71　(2)　46-46　2022/07

    Publisher: (NPO)日本口腔科学会

    ISSN： 0029-0297

    eISSN： 2185-0461

  32. 歯肉腫脹を主症状としたクローン病の1例

    伊藤 洋介, 高山 扶美子, 小笠原 貴子, 山座 治義, 増田 啓次, 廣藤 雄太, 千葉 雄太, 木舩 崇, 佐藤 綾子, 田中 絢子, 稲田 幸織, 福本 敏

    小児歯科学雑誌　60　(大会抄録号)　183-183　2022/03

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  33. サイトケラチンの網羅的解析による新たな歯原性上皮細胞マーカーの同定とその機能解析

    稲田 幸織, 千葉 雄太, 韓 旭, 佐藤 浩, 岡 桜恵, 福本 敏

    小児歯科学雑誌　60　(大会抄録号)　220-220　2022/03

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  34. S100a6がエナメル芽細胞分化に及ぼす影響

    大竹 慎司, 千葉 雄太, 吉岡 直哉, 室月 研, 山田 亜矢, 福本 敏, 齋藤 幹

    小児歯科学雑誌　60　(大会抄録号)　222-222　2022/03

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  35. 低年齢における重度乳歯外傷後の長期観察2例

    小笠原 貴子, 高山 扶美子, 佐藤 綾子, 木舩 崇, 増田 啓次, 廣藤 雄太, 千葉 雄太, 伊藤 洋介, 田中 絢子, 稲田 幸織, 山座 治義, 福本 敏

    小児歯科学雑誌　60　(地方会抄録号)　78-78　2022/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  36. COVID-19患者に歯科治療を施行した1例

    高山 扶美子, 山座 治義, 増田 啓次, 小笠原 貴子, 木舩 崇, 佐藤 綾子, 廣藤 雄太, 千葉 雄太, 伊藤 洋介, 田中 絢子, 稲田 幸織, 福本 敏

    小児歯科学雑誌　60　(地方会抄録号)　79-79　2022/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  37. Identification of pre-odontoblast specific GPI-anchored protein Lypd1 and it regulates cell differentiation in developing tooth

    FU Yao, 宮崎佳奈子, 千葉雄太, 吉崎恵悟, 鮒田啓太, 湯田智美, TIAN Tian, 水田敢士, 川原純平, 福本敏, 高橋一郎

    日本分子生物学会年会プログラム・要旨集(Web)　45th　2022

  38. Gタンパク質共役型受容体Gpr111/Adgrf2はエナメル質の石灰化を制御する(G-protein coupled receptor Gpr111/Adgrf2 regulates enamel mineralization)

    千葉 雄太, 吉崎 恵悟, 田 甜, 千葉 満生, 韓 旭, 稲田 幸織, 福本 敏

    Journal of Oral Biosciences Supplement　2021　110-110　2021/10

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  39. GPIアンカー型タンパク質Lypd1は象牙芽細胞分化に重要な役割を果たす(A GPI-anchored protein Lypd1 plays an important role in odontoblast differentiation during tooth development)

    傳 堯, 宮崎 佳奈子, 吉崎 恵悟, 千葉 雄太, 鮒田 啓太, 田 甜, 湯田 智美, 水田 敢士, 福本 敏, 高橋 一郎

    Journal of Oral Biosciences Supplement　2021　113-113　2021/10

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  40. 歯の発生に関わる新規細胞マーカー遺伝子の同定と機能解析

    千葉 雄太

    小児歯科学雑誌　59　(大会抄録(Web開催)号)　48-49　2021/05

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  41. 転写因子AmeloDが制御する新規エナメル質形成分子機序の解明

    賈 玲玲, 千葉 雄太, 吉崎 恵悟, 齋藤 幹, 福本 敏

    小児歯科学雑誌　59　(大会抄録(Web開催)号)　113-113　2021/05

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  42. Nephronectin regulates ameloblast differentiation through its RGD domain in tooth development

    Kanji Mizuta, Keigo Yoshizaki, Tomomi Yuta, Kanako Miyazaki, Keita Funada, Tian Tian, Yao Fu, Yuta Chiba, Ichiro Takahashi, Satoshi Fukumoto

    Protein Data Bank Symposium - 50th year celebration　2021/03

  43. 成熟期エナメル芽細胞におけるGタンパク質共役型受容体の機能解析

    千葉 雄太, 斎藤 幹, 吉崎 恵悟, 福本 敏

    Journal of Oral Biosciences Supplement　2020　148-148　2020/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  44. シングルセルRNAシーケンスによる歯胚遺伝子発現プロファイル

    千葉 雄太, 王 欣, 吉岡 直哉, 福本 敏

    Journal of Oral Biosciences Supplement　2020　367-367　2020/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  45. Transcriptome analysis of whole dental cells in developing tooth germ using single-cell RNA-sequence

    千葉雄太, 齋藤幹, 日野綾子, 新垣真紀子, 小山田優, 丸谷由里子, 山田亜矢, 福本敏, 福本敏

    小児歯科学雑誌　58　2020/09

    ISSN： 0583-1199

  46. 吸指癖の減少と不正咬合との関連性

    佐々木 桃子, 小山田 優, ただ野 愛実, 中村 友昭, 佐藤 優理亜, 星川 聖良, 千葉 満生, 山口 知子, 馬目 歩実, 千葉 雄太, 日野 綾子, 新垣 真紀子, 丸谷 由里子, 齋藤 幹, 山田 亜矢, 福本 敏

    小児歯科学雑誌　58　(地方会抄録号)　9-9　2020/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  47. Gタンパク質共役型受容体Gpr115はエナメル芽細胞における炭酸脱水素酵素の発現を制御しエナメル質形成に関与する

    千葉雄太, 齋藤幹, 吉崎恵悟, 福本敏, 福本敏

    Journal of Oral Biosciences Supplement (Web)　2019　152 (WEB ONLY)　2019/09

    ISSN： 2187-9109

  48. 内エナメル上皮の新規マーカーAmeloDの転写制御機構解明

    AL THAMIN Shahad, 千葉雄太, 吉崎恵悟, JIA LingLing, 山田亜矢, 齋藤幹, 福本敏

    小児歯科学雑誌　57　(2)　233-233　2019/05/01

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

  49. The G protein-coupled receptor Gpr115 regulates pH balance that is essential for tooth mineralization

    Yuta Chiba, Kan Saito, Aya Yamada, Fukumoto Satoshi

    The 11th Pediatric Dentistry Association of Asia 2018　2018/09

  50. 超高齢者の口腔悪性腫瘍切除術に対する全身麻酔経験ー適応とその判断ー

    柴田 菫, 千葉 雄太, 木村 瞳, 前川 翠, 的場 あつ子, 安田 真, 水田 健太郎

    第33回 東日本歯科麻酔学会 抄録集　2018/09

  51. 新規basic-helix-loop-helix転写因子AmeloDは歯原性上皮細胞の遊走能を制御し歯胚形態形成に関与する

    千葉 雄太, 吉崎 恵悟, 齋藤 幹, 中村 卓史, 岩本 勉, 福本 敏, He Bing, de Vega Susana, 石島 旨章, 山田 吉彦

    Journal of Oral Biosciences Supplement　2018　285-285　2018/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

  52. 歯冠・歯根長を制御する新規歯胚形態制御因子の同定と機能解明

    千葉 雄太, 齋藤 幹, 岩本 勉, 中村 卓史, 福本 敏

    小児歯科学雑誌　56　(2)　217-217　2018/04

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

  53. The role of the novel bHLH transcription factor AmeloD in tooth development Peer-reviewed

    千葉雄太

    東北大学 博士論文　2018/03

  54. Perlecan Regulates Pericyte Dynamics in the Repair Process of the Blood-Brain Barrier against Ischemic Stroke

    Nakamura K, Ikeuchi T, Zhang P, Rhodes C, Chiba Y, Ago T, Mukouyama YS, Yamada Y

    International Stroke Conference 2018　2018/01

  55. Perlecan is essential for the maintenance and repair of the blood-brain barrier against ischemic stroke through interacting with and activating pericytes.

    Nakamura K, Ikeuchi T, Zhang P, Rhodes C, Chiba Y, Ago T, Mukouyama YS, Yamada Y

    Neuroscience 2017　2017/11

  56. Pannexin 3 Deficiency in Mice Delays the Wound Healing Process

    Zhang, Peipei, Rhodes, Craig, Doyle, Andrew, Ishikawa, Masaki, Ikeuchi, Tomoko, Nakamura, Kuniyuki, Chiba, Yuta, Yamada, Yoshihiko

    PSRC 2017 62nd Annual Meeting　2017/04

  57. Epiprofin and T-box1 regulate the ameloblast lineage development

    Yuta Chiba, Kiyoshi Sakai, Tomoko Ikeuchi, Keigo Yoshizaki, Darius Mahboubi, Takashi Nakamura, Yoshihiko Yamada

    The International Association for Dental Research 2017 GENERAL SESSION　2017/03

  58. Perlecan Is Required for the Maintenance of the Blood-Brain Barrier through the Interaction with Pericytes in a Mouse Ischemic Stroke Model.

    Nakamura K, Ikeuchi T, Zhang P, Rhodes C, Chiba Y, Ago T, Mukouyama YS, Yamada Y

    International Stroke Conference 2017　2017/02

  59. 東日本大震災の被災地域における自己記入型食事調査票を用いた間食指導について

    山田 亜矢, 日野 綾子, 千葉 雄太, 馬目 歩実, 齋藤 幹, 福本 敏

    小児歯科学雑誌　55　(1)　81-81　2017/02

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  60. Epiprofin is a multi-functional factor essential to promote dental epithelial stem cell commitment to the ameloblast lineage and its proliferation and differentiation

    Yoshihiko Yamada, Kiyoshi Sakai, Yuta Chiba, Bing He, Darius Mahboubi, Craig Rhodes, Yasuo Yoshitomi, Satoshi Fukumoto, Takashi Nakamura

    The 2017 Japan-NIH Joint Symposium　2017

  61. The novel basic-Helix-Loop-Helix transcription factor AmeloD regulates tooth morphogenesis

    2017

  62. History of interactions between the NIH and Japanese scientists and the role of the novel bHLH transcription factor AmeloD in tooth development

    Yoshihiko Yamada, Yuta Chiba

    USJI seminar in NIH 2017　2017

  63. The G protein-coupled receptor Gpr115 regulates tooth mineralization

    Ryoko Takeuchi, Yuta Chiba, Tomoko Ikeuchi, Keigo Yoshizaki, Yoshihiko Yamada

    NIH SUMMER RESEARCH PROGRAM POSTER DAY 2017　2017

  64. Deficiency of Perlecan, a basement membrane heparan sulfate proteoglycan, leads to the blood-brain barrier deterioration in a mouse ischemic stroke model.

    Nakamura K, Zhang P, Ikeuchi T, Rhodes C, Mahboubi D, Chiba Y, Ago T, Mukouyama YS, Yamada Y

    Neuroscience 2016　2016/11

  65. 歯原性上皮細胞のエナメル芽細胞への分化におけるEpiprofinとT-box1の役割

    酒井 陽, 吉崎 恵悟, 千葉 雄太, 池内 友子, 山本 朗仁, 日比 英晴, 山田 吉彦

    Journal of Oral Biosciences Supplement　2016　357-357　2016/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

    eISSN： 2187-9109

  66. 組織再生に関わる基礎研究基盤の現状 エピプロフィンは歯原性上皮細胞のエナメル芽細胞系への誘導と分化を制御する多機能制御因子である

    山田 吉彦, 酒井 陽, 千葉 雄太, Mahboubi Darius, 池内 友子, 石河 真幸, 中村 卓史, 福本 敏

    Journal of Oral Biosciences Supplement　2016　57-58　2016/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

  67. S‐PRGフィラーの研磨材としての評価

    小野真理子, 日野綾子, 新垣真紀子, 菅原優, 鈴木真夕, 千葉雄太, 汲川利華, 齋藤幹, 山田亜矢, 福本敏

    小児歯科学雑誌　54　(1)　56-56　2016/02/25

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

    eISSN： 2186-5078

  68. Epfn and Tbx1 regulate dental epithelial stem cell fate to the ameloblast lineage

    Brittany Spivey, Yuta Chiba, Yoshihiko Yamada

    NIH SUMMER RESEARCH PROGRAM POSTER DAY 2016　2016

  69. 飲水時に引き起こされた乳歯の完全脱臼の2例

    千葉雄太, 齋藤幹, 成瀬正啓, 日野綾子, 山田亜矢, 福本敏

    小児歯科学雑誌　53　(1)　103-103　2015/02/25

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

  70. 歯胚形成におけるビタミンDの役割

    池内 友子, 千葉 雄太, 成瀬 正啓, 新垣 真紀子, 中村 卓史, 福本 敏

    小児歯科学雑誌　51　(2)　270-270　2013/04/25

    Publisher: (公社)日本小児歯科学会

    ISSN： 0583-1199

  71. The role of Gb4 during tooth development

    Yuta Chiba, Takashi Nakamura, Naruse Masahiro, Satoshi Fukumoto

    The 24th International Congress of International Association of Pediatric Dentistry　2013

  72. 歯の発生におけるスフィンゴ糖脂質の役割

    千葉 雄太, 中村 卓史, 成瀬 正啓, 池内 友子, 新垣 真紀子, 福本 敏

    Journal of Oral Biosciences Supplement　2012　108-108　2012/09

    Publisher: (一社)歯科基礎医学会

    ISSN： 2187-2333

Show all ︎Show first 5

Books and Other Publications 5

  1. 日本歯科評論 「臨床に向けた最近の動向から 歯特異的遺伝子の同定から歯の形成機構の理解まで（３） ──エナメル質石灰化のメカニズム解明を目指して」

    千葉雄太・齋藤 幹・山田亜矢・福本 敏

    ヒョーロン・パブリッシャーズ社　2026/03

  2. 日本歯科評論「臨床に向けた最近の動向から 歯特異的遺伝子の同定から歯の形成機構の理解まで（２） ──歯胚に特異的に発現する転写因子の同定と機能解析」

    岡 桜恵, 千葉雄太, 佐藤 浩, 千葉満生, 福本 敏

    ヒョーロン・パブリッシャーズ社　2026/02

  3. 日本歯科評論「臨床に向けた最近の動向から 歯特異的遺伝子の同定から歯の形成機構の理解まで（1） ──歯に表現系を示す遺伝性疾患の解明に向けて」

    島田 茜, 山田亜矢, 千葉雄太, 齋藤 幹, 福本 敏

    ヒョーロン・パブリッシャーズ社　2026/01

  4. 月刊 細胞 「歯の発生および再生」

    福本敏, 吉崎恵悟, 千葉雄太, 新垣真紀子, 山田亜矢, 齋藤幹

    ニュー・サイエンス社　2018/09

  5. 月刊内分泌・糖尿病・代謝内科 「新規転写因子エピプロフィンによる副甲状腺ホルモン発現制御」

    中村卓史, 福本敏, 中村はな, 千葉雄太, 山田吉彦, 岩本容泰

    科学評論社　2014/02

Presentations 19

  1. Uncovering pathogenesis of dental anomalies using tooth germ cDNA library Invited

    Yuta Chiba

    2025 TU-HKU-FJMU International Symposium on Oral Health Sciences　2025/10/13

  2. 〜お口からはじめる健康づくり〜乳幼児期の特徴とオーラル・ケアについて Invited

    千葉雄太

    令和６年度第２回多賀城市こども家庭センター従事者研修会　2024/12/04

  3. Genetic Disorders and Dental Anomalies in Pediatric Dentistry Invited

    Yuta Chiba

    Universitas Gadjah Mada Dental Summer Course 2024　2024/07/16

  4. シングルセルRNAシークエンスを基盤とした歯の発生機構解明と疾患機序探索への応用 Invited

    千葉雄太

    第62回日本小児歯科学会大会 受賞講演　2024/05/19

  5. 医師臨床研修制度の概要 Invited

    千葉雄太

    第29回NPO法人艮陵協議会 臨床研修指導医講習会　2023/09/16

  6. 医師臨床研修制度の概要と直近の制度改正について Invited

    千葉雄太

    第28回NPO法人艮陵協議会 臨床研修指導医講習会　2023/02/11

  7. 医師臨床研修制度の理念・概要と最近の動向 Invited

    千葉雄太

    第27回NPO法人艮陵協議会 臨床研修指導医講習会　2022/09/17

  8. 歯が生える前からの口腔育成について Invited

    千葉 雄太

    第32回福岡母子総合研究シンポジウム 第19回市民公開講座　2022/08/27

  9. シングルセルRNAシークエンスを用いた 歯の発生基盤の解明と再生医療への応用 Invited

    千葉 雄太, 福本 敏

    第76回NPO法人日本口腔科学会学術集会 シンポジウム　2022/04/23

  10. Identification and functional analysis of novel genes from developing tooth germ Invited

    Yuta Chiba

    The 31st Fukuoka Inernational Symposium on Pediatric/Maternal-child health research (FISP/M)　2021/08/28

  11. Single-cell RNA-seq profiling of the dental epithelium in the ever-growing mouse incisor Invited

    Yuta Chiba

    The 99th General Session of IADR 2021 SYMPOSIA　2021/07/21

  12. 歯の発生に関わる新規細胞マーカー遺伝子の同定と機能解析 Invited

    千葉雄太

    第59回日本小児歯科学会大会 受賞講演　2021/06/06

  13. 成熟期エナメル芽細胞におけるGタンパク質共役型受容体の機能解析

    千葉雄太、齋藤幹、吉崎恵悟、福本敏

    第62回歯科基礎医学会学術大会 アップデートシンポジウム　2020/10/08

  14. The G-protein coupled receptor Gpr115 is essential for enamel mineralization via regulation of pH homeostasis

    Yuta Chiba, Keigo Yoshizaki, Tomoko Ikeuchi, Kan Saito, Craig Rhodes, Tsutomu Iwamoto, Takashi Nakamura, Yoshihiko Yamada, Satoshi Fukumoto

    NIH-Japan-JSPS symposium 2019　2019/10/28

  15. 大学院から広がる人との繋がり 〜研究編〜 Invited

    千葉雄太

    東北大学歯学部５年次 合同講義「ダイバーシティ歯学論」　2019/07/10

  16. Identification of the tooth-specific novel transcription factor AmeloD and its role during tooth development

    Yuta Chiba, Kan Saito, Takashi Nakamura, Yoshihiko Yamada, Satoshi Fukumoto

    The Kick-off Symposium of Advanced Graduate Program for Future Medicine and Health Care in Tohoku University　2019/03/05

  17. 新規bHLH転写因子AmeloDの同定と歯の発生過程における役割

    千葉 雄太, 山田吉彦, 福本敏

    第４回口腔医科学フロンティア研究会　2019/03/04

  18. 大学院から広がる人との繋がり ～留学編～ Invited

    千葉雄太

    東北大学歯学部５年次 合同講義「科学から広がる人との繋がり ～一度きりの人生をより楽しむために～」　2018/07/18

  19. The role of the novel bHLH transcription factor AmeloD in tooth morphogenesis

    Yuta Chiba

    2017/11/03

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Research Projects 11

  1. 空間オミクス解析で解き明かすエナメル芽細胞の周期的分化スイッチング機構

    齋藤幹, 千葉雄太

    System: 日本学術振興会 科学研究費助成事業 挑戦的研究(萌芽)

    2026/07 - 2028/06

  2. 象牙質形成における骨形成因子と歯髄幹細胞ニッチとの相互作用解明

    丸谷由里子, 千葉雄太

    System: 日本学術振興会 科学研究費助成事業 基盤研究(C)

    2025/04 - 2028/03

  3. サイトケラチン発現制御による歯原性上皮細胞分化誘導技術の開発

    千葉雄太

    System: 日本学術振興会 科学研究費助成事業 若手研究

    2025/04 - 2028/03

  4. シングルセル解析を基盤とした歯の先天異常発生メカニズムの解明

    千葉雄太、福本敏、吉崎恵悟

    Offer Organization: 公益財団法人富徳会

    System: フォローアップ助成

    2024/12 - 2027/11

  5. 組織再生誘導技術開発を目指した上皮器官形態形成と免疫クロストークの解明

    山田 亜矢, 吉崎 恵悟, 福本 敏, 千葉 雄太

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 基盤研究(B)

    Institution: 東北大学

    2024/04 - 2027/03

  6. Elucidation of molecular mechanism of enamel formation and application to non-cellular hard tissue regeneration

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

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

    Institution: Kyushu University

    2022/04 - 2027/03

  7. 唾液腺発生における神経-器官相互作用の分子機構の解明と機能再生技術への応用

    中村 卓史、若森実、中村はな、真藤裕基、千葉雄太

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業 国際共同研究加速基金(国際共同研究強化(B))

    Category: 国際共同研究加速基金(国際共同研究強化(B))

    Institution: 東北大学

    2021/10 - 2025/03

    More details Close

    歯、毛包、腺組織、腎臓、肺、消化管組織に存在する上皮組織は、共通性のある上皮間葉相互作用により発生し、転写因子エピプロフィン（Epfn）は上皮細胞の増殖、枝分かれ、運命決定、組織幹細胞維持、細胞死を制御し上皮組織の発生形態形成、また皮膚、毛包などでは組織恒常性維持のため幹細胞維持とTransient-amplifying (TA)細胞の増殖と運命決定に重要である。完成した器官が、支配神経制御下で生体機能を発揮するためには、器官形成時に神経終末が効果器となる細胞（唾液腺では主に筋上皮細胞）に隣接して分化誘導され組織内に配置される必要がある。すなわち自律神経制御を受ける唾液腺は、器官完成後分泌を促進させる指令を出す副交感神経とその指令を受け唾液を分泌させるために腺房・導管を収縮させる筋上皮細胞が近接されて器官設計されることが必要である。これらの器官形成には、歯、毛包、腺組織、腎臓、肺、消化管組織形成期に展開される共通性のある上皮間葉相互作用が重要である。転写因子エピプロフィン（Epfn）は上皮細胞の増殖、枝分かれ、運命決定、組織幹細胞維持、細胞死を制御しているが、神経―上皮組織間の相互作用にも関与している事が、強く示唆される結果を得た。本研究の目的は、唾液腺器官培養系を用いて神経伝達物質とEpfnがどのように共役し、唾液腺上皮細胞の増殖と運命決定と組織内の細胞配置を制御しているのかを解明することであり、海外共同研究では、放射線照射モデルを利用し、障害唾液腺の再生を発生過程での神経伝達物質とEpfnの作用を応用することによる効果的で機能的な再生器官誘導法樹立への道筋をたてることである。

  8. The role of orphan G-protein coupled receptor Gpr115 during tooth development

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists

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

    Institution: Tohoku University

    2020/04 - 2023/03

  9. 新規歯胚形態形成因子AmeloDに関わる遺伝子制御機構解明

    千葉雄太

    System: 公益財団法人富徳会研究助成金

    2019/04 - 2020/03

  10. The role of novel basic-helix-loop-helix transcription factor AmeloD during tooth development

    Chiba Yuta

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity start-up

    Category: Grant-in-Aid for Research Activity start-up

    Institution: Tohoku University

    2018/08 - 2020/03

    More details Close

    Organ-specific basic-Helix-Loop-Helix (bHLH) factors, such as MyoD and NeuroD, have essential roles in organ development processes. However, tooth-specific bHLH factor has not been reported yet. The aim of this study is identification of the tooth-specific bHLH factor. We screened the bHLH family expressed in tooth germ cDNA library and identified the novel bHLH factor, AmeloD. In vivo and in vitro analyses using AmeloD knockout mouse revealed that AmeloD plays essential role in tooth morphogenesis. AmeloD was expressed in inner dental epithelium, the ameloblast progenitor cell. AmeloD promoted migration of inner enamel epithelium via suppression of transcriptional activity of E-cadherin, a cell adhesion molecule. Thus, AmeloD is a novel bHLH factor essential for tooth development processes.

  11. Functional analysis of cell-cell junction molecule toward artificial enamel formation

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research Grant-in-Aid for JSPS Fellows

    Category: Grant-in-Aid for JSPS Fellows

    Institution: Tohoku University

    2015/04 - 2018/03

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Teaching Experience 9

  1. 小児歯科学　東北大学歯学部

  2. 小児歯科技工学　仙台歯科技工士専門学校

  3. 臨床実習主任（小児歯科）　東北大学歯学部

  4. 口腔保健発育学III 小児歯科学実習主任　東北大学歯学部

  5. 歯科臨床ゼミ主任（小児歯科）　東北大学歯学部

  6. 小児歯科技工学　東北歯科技工専門学校

  7. 歯科臨床ゼミ主任（小児歯科）　東北大学歯学部

  8. 口腔保健発育学III 小児歯科学実習主任　東北大学歯学部

  9. 小児歯科技工学　東北歯科技工専門学校

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Social Activities 3

  1. 塩釜市・多賀城市 乳幼児歯科健診（2歳半）担当歯科医師

    2024/04 - Present

  2. 仙台市・多賀城市 保育園嘱託歯科医

    2024/04 - Present

  3. 福岡市 乳幼児歯科健診（1歳半健診）担当歯科医師

    2021/04 - 2022/03

Media Coverage 3

  1. Front cover, Journal of Dental Research (Vol. 105, No. 5)

    https://journals.sagepub.com/toc/jdrb/105/5 (Keratin 15 Regulates Cell Proliferation in Outer Enamel Epithelium)

    2026/05

    Type: Promotional material

  2. Dentalism News & Topics - エナメル質の石灰化を制御する受容体を同定

    Dentalism 45号

    2021/05

    Type: Newspaper, magazine

  3. エナメル質の形成に関する受容体を特定—東北大

    日本歯科新聞

    2020/11/17

    Type: Newspaper, magazine

Academic Activities 2

  1. Journal of Dental Research Editorial Board Member

    2023/01/01 - Present

  2. Frontiers in Dental Medicine Associate Editor

    2021/02/01 - Present