Details of the Researcher

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Akiko Ogawa
Section
Graduate School of Pharmaceutical Sciences
Job title
Associate Professor
Degree

  • 博士（医学）（熊本大学）

Research History 6

  • 2025/04 - Present
    東北大学大学院薬学研究科・薬学部　准教授

  • 2023/04 - Present
    創発研究者

  • 2021/11 - Present
    熊本大学大学院 生命科学研究部 眼科学講座　客員講師

  • 2019/10 - 2025/03
    Tohoku University, Institute of Development, Aging and Cancer　Assistant Professor

  • 2014/04 - 2021/10
    Kumamoto University

  • 2012/04 - 2014/03
    東京厚生年金病院（JCHO東京新宿メディカルセンター）　初期研修医

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Education 2

  • Kumamoto University　Graduate School of Medical Sciences

    2015/04 - 2019/03

  • The University of Tokyo　Faculty of Medicine　School of Medicine

    2006/04 - 2012/03

Professional Memberships 6

  • 日本痛風・尿酸核酸学会

  • 日本生化学会

  • THE RNA SOCIETY OF JAPAN

  • THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

  • JAPAN GLAUCOMA SOCIETY

  • JAPANESE OPHTHALMOLOGICAL SOCIETY

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Research Interests 5

  • RNA

  • GPCR

  • glaucoma

  • Metabolism

  • Ophthalmology

Research Areas 2

  • Life sciences / Cell biology /

  • Life sciences / Ophthalmology / Glaucoma

Awards 24

  1. 第 11 回がんと代謝研究会 IN 草津

    2025/05　最優秀ポスター賞

  2. 2024年度 野口遵賞

    2025/03

  3. 第19回 生命医科学研究所ネットワーク国際シンポジウム Best Oral Presentation Award

    2024/10

  4. 第７回 東北大学優秀女性研究者賞 紫千代萩賞（医歯薬学・保健部門）

    2024/03　東北大学　エピトランスクリプトームによる生体代謝研究

  5. 日本痛風・尿酸核酸学会 優秀論文賞

    2024/02　日本痛風・尿酸核酸学会

  6. 2023年度 日本医師会医学研究奨励賞

    2023/11　日本医師会

  7. 第34回日本緑内障学会 学会長企画 新進気鋭の緑内障研究者の競演 Gold賞（第1位）

    2023/09　日本緑内障学会

  8. JCA2023 Woman Scientist Plenary Symposium Award

    2023/09　日本癌学会

  9. 第56回日本痛風・尿酸核酸学会総会 最優秀演題賞

    2023/02

  10. 東北大学 プロミネントリサーチフェロー

    2023

  11. 第3回北澤克明記念緑内障学研究助成(北澤賞)

    2023

  12. 第15回資生堂女性研究者サイエンスグラント

    2022/06

  13. 2022年度アステラス病態代謝研究会 優秀発表賞

    2022

  14. 東北医学会奨学賞（A）

    2022/01

  15. 第11回参天製薬創業者記念眼科医学研究基金

    2021/12

  16. 第 28回 加齢医学研究所研究奨励賞

    2021/01

  17. 第37回 加齢医学研究所集談会コンテスト第１位

    2020/07

  18. 公益信託三島済一記念眼科研究国際交流基金 国内眼科医学研究者

    2019/08

  19. 公益信託三島済一記念眼科研究国際交流基金 国内眼科医学研究者(三島賞)

    2019/07

  20. 熊本大学眼科学術奨励賞

    2019/03

  21. 須田記念緑内障治療研究奨励基金

    2019/03

  22. 熊本大学女性研究者奨励賞

    2019/02

  23. 日本緑内障学会EGSフェローシップグラント（13th European Glaucoma Society Congress）

    2018/05

  24. 第39回日本分子生物学会年会 優秀ポスター賞

    2016/12

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Papers 19

  1. Mitochondrial translation regulates terminal erythroid differentiation by maintaining iron homeostasis. International-journal

    Tatsuya Morishima, Md Fakruddin, Yohei Kanamori, Takeshi Masuda, Akiko Ogawa, Yuxin Wang, Vivien A C Schoonenberg, Falk Butter, Yuichiro Arima, Takaaki Akaike, Toshiro Moroishi, Kazuhito Tomizawa, Toshio Suda, Fan-Yan Wei, Hitoshi Takizawa

    Science advances　11　(8)　eadu3011　2025/02/21

    DOI： 10.1126/sciadv.adu3011 　

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    Mitochondrial tRNA taurine modifications mediated by mitochondrial tRNA translation optimization 1 (Mto1) is essential for the mitochondrial protein translation. Mto1 deficiency was shown to induce proteostress in embryonic stem cells. A recent finding that a patient with MTO1 gene mutation showed severe anemia led us to hypothesize that Mto1 dysfunctions may result in defective erythropoiesis. Hematopoietic-specific Mto1 conditional knockout (cKO) mice were embryonic lethal and showed niche-independent defect in erythroblast proliferation and terminal differentiation. Mechanistically, mitochondrial oxidative phosphorylation complexes were severely impaired in the Mto1 cKO fetal liver, and this was followed by cytosolic iron accumulation. Overloaded cytosolic iron promoted heme biosynthesis, which induced an unfolded protein response (UPR) in Mto1 cKO erythroblasts. An iron chelator or UPR inhibitor rescued erythroid terminal differentiation in the Mto1 cKO fetal liver in vitro. This mitochondrial regulation of iron homeostasis revealed the indispensable role of mitochondrial tRNA modification in fetal hematopoiesis.

  2. Structural insights into the agonist selectivity of the adenosine A3 receptor. International-journal

    Hidetaka S Oshima, Akiko Ogawa, Fumiya K Sano, Hiroaki Akasaka, Tomoyoshi Kawakami, Aika Iwama, Hiroyuki H Okamoto, Chisae Nagiri, Fan-Yan Wei, Wataru Shihoya, Osamu Nureki

    Nature communications　15　(1)　9294-9294　2024/11/07

    DOI： 10.1038/s41467-024-53473-1 　

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    Adenosine receptors play pivotal roles in physiological processes. Adenosine A3 receptor (A3R), the most recently identified adenosine receptor, is expressed in various tissues, exhibiting important roles in neuron, heart, and immune cells, and is often overexpressed in tumors, highlighting the therapeutic potential of A3R-selective agents. Recently, we identified RNA-derived N6-methyladenosine (m6A) as an endogenous agonist for A3R, suggesting the relationship between RNA-derived modified adenosine and A3R. Despite extensive studies on the other adenosine receptors, the selectivity mechanism of A3R, especially for A3R-selective agonists such as m6A and namodenoson, remained elusive. Here, we identify tRNA-derived N6-isopentenyl adenosine (i6A) as an A3R-selective ligand via screening of modified nucleosides against the adenosine receptors. Like m6A, i6A is found in the human body and may be an endogenous A3R ligand. Our cryo-EM analyses elucidate the A3R-Gi complexes bound to adenosine, 5'-N-ethylcarboxamidoadenosine (NECA), m6A, i6A, and namodenoson at overall resolutions of 3.27 Å (adenosine), 2.86 Å (NECA), 3.19 Å (m6A), 3.28 Å (i6A), and 3.20 Å (namodenoson), suggesting the selectivity and activation mechanism of A3R. We further conduct structure-guided engineering of m6A-insensitive A3R, which may aid future research targeting m6A and A3R, providing a molecular basis for future drug discovery.

  3. Pathological mutations promote proteolysis of mitochondrial tRNA-specific 2-thiouridylase 1 (MTU1) via mitochondrial caseinolytic peptidase (CLPP). International-journal

    Raja Norazireen Raja Ahmad, Long-Teng Zhang, Rikuri Morita, Haruna Tani, Yong Wu, Takeshi Chujo, Akiko Ogawa, Ryuhei Harada, Yasuteru Shigeta, Kazuhito Tomizawa, Fan-Yan Wei

    Nucleic acids research　52　(3)　1341-1358　2024/02/09

    DOI： 10.1093/nar/gkad1197 　

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    MTU1 controls intramitochondrial protein synthesis by catalyzing the 2-thiouridine modification of mitochondrial transfer RNAs (mt-tRNAs). Missense mutations in the MTU1 gene are associated with life-threatening reversible infantile hepatic failure. However, the molecular pathogenesis is not well understood. Here, we investigated 17 mutations associated with this disease, and our results showed that most disease-related mutations are partial loss-of-function mutations, with three mutations being particularly severe. Mutant MTU1 is rapidly degraded by mitochondrial caseinolytic peptidase (CLPP) through a direct interaction with its chaperone protein CLPX. Notably, knockdown of CLPP significantly increased mutant MTU1 protein expression and mt-tRNA 2-thiolation, suggesting that accelerated proteolysis of mutant MTU1 plays a role in disease pathogenesis. In addition, molecular dynamics simulations demonstrated that disease-associated mutations may lead to abnormal intermolecular interactions, thereby impairing MTU1 enzyme activity. Finally, clinical data analysis underscores a significant correlation between patient prognosis and residual 2-thiolation levels, which is partially consistent with the AlphaMissense predictions. These findings provide a comprehensive understanding of MTU1-related diseases, offering prospects for modification-based diagnostics and novel therapeutic strategies centered on targeting CLPP.

  4. Activation of the urotensin-II receptor by remdesivir induces cardiomyocyte dysfunction. International-journal

    Akiko Ogawa, Seiya Ohira, Yuri Kato, Tatsuya Ikuta, Shota Yanagida, Xinya Mi, Yukina Ishii, Yasunari Kanda, Motohiro Nishida, Asuka Inoue, Fan-Yan Wei

    Communications biology　6　(1)　511-511　2023/05/12

    DOI： 10.1038/s42003-023-04888-x 　

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    Remdesivir is an antiviral drug used for COVID-19 treatment worldwide. Cardiovascular side effects have been associated with remdesivir; however, the underlying molecular mechanism remains unknown. Here, we performed a large-scale G-protein-coupled receptor screening in combination with structural modeling and found that remdesivir is a selective, partial agonist for urotensin-II receptor (UTS2R) through the Gαi/o-dependent AKT/ERK axis. Functionally, remdesivir treatment induced prolonged field potential and APD90 in human induced pluripotent stem cell (iPS)-derived cardiomyocytes and impaired contractility in both neonatal and adult cardiomyocytes, all of which mirror the clinical pathology. Importantly, remdesivir-mediated cardiac malfunctions were effectively attenuated by antagonizing UTS2R signaling. Finally, we characterized the effect of 110 single-nucleotide variants in UTS2R gene reported in genome database and found four missense variants that show gain-of-function effects in the receptor sensitivity to remdesivir. Collectively, our study illuminates a previously unknown mechanism underlying remdesivir-related cardiovascular events and that genetic variations of UTS2R gene can be a potential risk factor for cardiovascular events during remdesivir treatment, which collectively paves the way for a therapeutic opportunity to prevent such events in the future.

  5. Protocol for preparation and measurement of intracellular and extracellular modified RNA using liquid chromatography-mass spectrometry. International-journal

    Akiko Ogawa, Fan-Yan Wei

    STAR protocols　2　(4)　100848-100848　2021/12/17

    DOI： 10.1016/j.xpro.2021.100848 　

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    About 150 modifications have been identified in RNA species. Besides their regulatory roles in the intracellular gene expression, abundant modified RNA nucleosides are catabolized from RNA and released into extracellular fluids, which can impact extracellular signaling as ligands for receptors. Here, we describe a protocol to prepare samples from biological specimens, including cultured cells, extracellular fluid, and tissues, to measure both intracellular and extracellular RNA modifications using mass spectrometry. For complete details on the use and execution of this protocol, please refer to Ogawa et al. (2021).

  6. 緑内障術後線維化におけるRNA修飾の変動

    小川 亜希子, 井上 俊洋, 魏 范研

    日本緑内障学会抄録集　32回　76-76　2021/09

    Publisher: 日本緑内障学会

  7. Potential roles of the IL-6 family in conjunctival fibrosis. International-journal

    Fumika Watanabe-Kitamura, Akiko Ogawa, Tomokazu Fujimoto, Satoshi Iraha, Miyuki Inoue-Mochita, Takahiro Watanabe, Eri Takahashi, Hidenobu Tanihara, Toshihiro Inoue

    Experimental eye research　210　108708-108708　2021/07/30

    DOI： 10.1016/j.exer.2021.108708 　

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    Elevated intraocular pressure (IOP) is a significant risk factor for vision loss due to glaucoma, which is a major cause of blindness worldwide. Glaucoma filtration surgery (GFS) is an important method to reduce IOP by guidance of aqueous humor into a newly built filtration bleb in the conjunctiva; management of the wound healing mechanism is essential for the success of GFS. Here, we investigated the roles of interleukin (IL)-6 family members during the wound healing process after GFS. At the surgical site, the expression levels of genes encoding IL-6, oncostatin M (OSM), their receptors, and collagen I were elevated at 3 h after GFS, whereas the levels of genes encoding transforming growth factor (TGF)-β, α-smooth muscle actin (SMA), type IV collagen, and fibronectin were elevated at 3 days after GFS. IL-6 trans-signaling and OSM signaling suppressed TGF-β-induced expression of α-SMA and collagen IV, as well as activation of the non-canonical TGF-β pathway, suggesting that IL-6 and OSM may aid in controlling the phase transition from inflammation to proliferation and remodeling. The suppressive effects of OSM were accompanied by STAT3 activation, such that STAT1 function was complementary to STAT3. Taken together, these observations indicated that IL-6 family members constitute early response genes after GFS, which can suppress TGF-β-induced expression of late response genes at the surgical site after GFS.

  8. 落屑緑内障に対するBaerveldtチューブシャント手術の成績

    松村 智世, 中島 圭一, 高橋 枝里, 米村 瞳, 二口 亜希子, 谷原 秀信, 井上 俊洋

    日本眼科学会雑誌　125　(2)　111-116　2021/02

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  9. N6-methyladenosine (m6A) is an endogenous A3 adenosine receptor ligand. International-journal

    Akiko Ogawa, Chisae Nagiri, Wataru Shihoya, Asuka Inoue, Kouki Kawakami, Suzune Hiratsuka, Junken Aoki, Yasuhiro Ito, Takeo Suzuki, Tsutomu Suzuki, Toshihiro Inoue, Osamu Nureki, Hidenobu Tanihara, Kazuhito Tomizawa, Fan-Yan Wei

    Molecular cell　81　(4)　659-674　2021/01/12

    DOI： 10.1016/j.molcel.2020.12.038 　

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    About 150 post-transcriptional RNA modifications have been identified in all kingdoms of life. During RNA catabolism, most modified nucleosides are resistant to degradation and are released into the extracellular space. In this study, we explored the physiological role of these extracellular modified nucleosides and found that N6-methyladenosine (m6A), widely recognized as an epigenetic mark in RNA, acts as a ligand for the human adenosine A3 receptor, for which it has greater affinity than unmodified adenosine. We used structural modeling to define the amino acids required for specific binding of m6A to the human A3 receptor. We also demonstrated that m6A was dynamically released in response to cytotoxic stimuli and facilitated type I allergy in vivo. Our findings implicate m6A as a signaling molecule capable of activating G protein-coupled receptors (GPCRs) and triggering pathophysiological responses, a previously unreported property of RNA modifications.

  10. Correction: TGF-β-induced activation of conjunctival fibroblasts is modulated by FGF-2 and substratum stiffness. International-journal

    Tomoyo Matsumura, Tomokazu Fujimoto, Satoshi Iraha, Akiko Futakuchi, Yuji Takihara, Fumika Watanabe-Kitamura, Eri Takahashi, Miyuki Inoue-Mochita, Hidenobu Tanihara, Toshihiro Inoue

    PloS one　16　(5)　e0251615　2021

    DOI： 10.1371/journal.pone.0251615 　

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    [This corrects the article DOI: 10.1371/journal.pone.0242626.].

  11. Intraocular pressure-lowering effects of ripasudil in uveitic glaucoma, exfoliation glaucoma, and steroid-induced glaucoma patients: ROCK-S, a multicentre historical cohort study. International-journal Peer-reviewed

    Akiko Futakuchi, Takeshi Morimoto, Yoko Ikeda, Hidenobu Tanihara, Toshihiro Inoue

    Scientific reports　10　(1)　10308-10308　2020/06/25

    DOI： 10.1038/s41598-020-66928-4 　

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    To evaluate the efficacy and safety of ripasudil for treatment of secondary glaucoma, a historical cohort study was conducted at 18 centres in Japan. Adults (age ≥20 years) who needed additional IOP reduction and received topical 0.4% ripasudil between 2014 and 2018 due to three secondary glaucoma subtypes, including uveitic glaucoma (UG), exfoliation glaucoma (EG) or steroid-induced glaucoma (SG) were assessed for mean IOP change from baseline prior to additional treatment with ripasudil. We further evaluated the IOP change in each glaucoma subtype, baseline characteristics of each cohort, course of uveitis-induced inflammation in UG eyes, and proportion of patients in each cohort with adverse events. In 332 eyes from 332 patients eligible for this study, the mean overall IOP reductions from baseline at 1, 3, and 6 months were -5.86 ± 9.04 mmHg (-19.4 ± 25.1%), -6.18 ± 9.03 mmHg (-20.0 ± 27.1%), and -7.00 ± 8.60 mmHg (-23.4 ± 25.6%), respectively. These changes were all statistically significant. Of 332 eyes, 109 eyes had UG, 181 had EG, and 42 eyes had SG. The IOP-lowering effects of ripasudil in UG and SG were significantly greater than those of EG at every time point. This finding could have been related to higher baseline IOP levels in UG and SG. UG patients exhibited significant decreases in mean cell score of the anterior segment after ripasudil treatment. No severe adverse events were reported. These findings suggest that treatment with ripasudil is a safe and effective therapeutic modality for IOP reduction in secondary glaucoma.

  12. TGF-β-induced activation of conjunctival fibroblasts is modulated by FGF-2 and substratum stiffness. International-journal

    Tomoyo Matsumura, Tomokazu Fujimoto, Akiko Futakuchi, Yuji Takihara, Fumika Watanabe-Kitamura, Eri Takahashi, Miyuki Inoue-Mochita, Hidenobu Tanihara, Toshihiro Inoue

    PloS one　15　(11)　e0242626　2020

    DOI： 10.1371/journal.pone.0242626 　

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    PURPOSE: This study aimed to investigate the effects of substratum stiffness on the sensitivity of human conjunctival fibroblasts to transforming growth factor (TGF)-β, and to explore the molecular mechanism of action. METHODS: Human conjunctival fibroblasts were cultured on collagen-coated plastic or silicone plates. The stiffness of the silicone plates was 0.2 or 64 kPa. Cells were treated by 2.5 ng/mL TGF-β2 with or without fibroblast growth factor (FGF)-2 (0-100 ng/mL) for 24 h or 48 h. The protein expression levels were determined by Western blot analysis. Cell proliferation was assessed using the WST-8 assay. RESULTS: FGF-2 suppressed the TGF-β-induced expression of α-smooth muscle actin (SMA) and collagen type I (Col I), but not fibronectin (FN). Both FGF-2 and TGF-β2 increased cell proliferation without an additive effect. The induction of α-SMA by TGF-β2 was decreased on the soft substratum, without any change in the expression level or subcellular location of Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ). FGF-2 suppressed TGF-β-induced α-SMA expression even on the soft substratum. CONCLUSIONS: FGF-2 treatment and a soft substratum suppressed TGF-β-induced transdifferentiation of conjunctival fibroblasts into myofibroblasts. FGF-2 attenuated the TGF-β-induced expression of α-SMA, even on a soft substratum.

  13. DNA methyltransferase inhibitor suppresses fibrogenetic changes in human conjunctival fibroblasts. International-journal Peer-reviewed

    Hitomi Yonemura, Akiko Futakuchi, Miyuki Inoue-Mochita, Tomokazu Fujimoto, Eri Takahashi, Hidenobu Tanihara, Toshihiro Inoue

    Molecular vision　25　382-390　2019

    eISSN： 1090-0535

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    Purpose: This study aimed to clarify the effects of a DNA methyltransferase inhibitor on fibrogenetic changes in human conjunctival fibroblasts (HConF). Methods: HConF were pretreated with the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-Aza-dC) for 48 h. After one passage, the cells were treated with 5 ng/ml of transforming growth factor (TGF)-β2 for 48 h, and the expression levels of α-smooth muscle actin (α-SMA), extracellular matrix proteins, and phosphorylated Smad3 were evaluated with western blotting. A fusion construct between the COL1A2 promoter and the luciferase gene was introduced into the HConF after the first passage, and the construct's activity was detected via a luciferase reporter gene assay. Results: TGF-β2-induced upregulation of α-SMA was suppressed by pretreatment with 5-Aza-dC (0.1, 1.0, and 10 μM) in a dose-dependent manner. Upregulation of type I collagen was also suppressed by 10 μM 5-Aza-dC pretreatment. In contrast, 5-Aza-dC had no inhibitory effect on the expression of fibronectin or phosphorylated Smad3. However, COL1A2 promoter activity was suppressed with 5-Aza-dC pretreatment. Conclusions: In HConF, fibrogenetic changes were partly suppressed with a DNA methyltransferase inhibitor, suggesting an indirect inhibitory effect of the inhibitor on the COL1A2 promoter in HConF.

  14. Interleukin-6-mediated trans-signaling inhibits transforming growth factor-β signaling in trabecular meshwork cells. International-journal Peer-reviewed

    Miyuki Inoue-Mochita, Toshihiro Inoue, Sachi Kojima, Akiko Futakuchi, Tomokazu Fujimoto, Saori Sato-Ohira, Utako Tsutsumi, Hidenobu Tanihara

    The Journal of biological chemistry　293　(28)　10975-10984　2018/07/13

    DOI： 10.1074/jbc.RA118.003298 　

    ISSN： 0021-9258

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    Glaucoma is one of the major causes of blindness, and transforming growth factor-β2 (TGF-β2) has been found to be elevated in the aqueous humor of eyes with primary open-angle glaucoma (POAG). TGF-β2 in aqueous humor causes the glaucoma-related fibrosis of human trabecular meshwork (HTM), suggesting an important role of TGF-β in POAG pathogenesis. Here, we sought to elucidate the effects of IL-6 trans-signaling on TGF-β signaling in HTM cells. Using a multiplex immunoassay, POAG patients decreased IL-6 levels and increased soluble IL-6 receptor (sIL-6R) levels compared with the controls. In in vitro experiments, we observed that the IL-6 level was increased in the conditioned medium of HTM cells after TGF-β2 stimulation. To elucidate the relationship between TGF-β2 and IL-6 in HTM cells, we conducted Western blotting and immunohistochemical analyses, and we noted that the combination of IL-6 and sIL-6R (IL6/sIL-6R) suppressed TGF-β-induced up-regulation of α-smooth muscle actin in HTM cells, whereas IL-6 alone did not. This suggests that trans-signaling, not classic signaling, of IL-6 suppresses TGF-β-induced fibrosis of HTM. IL6/sIL-6R also suppressed TGF-β-mediated activation of myosin light chain 2 (MLC2), Smad2, and p38. Of note, these inhibitory effects of IL6/sIL-6R on TGF-β were partly reduced by siRNA-mediated knockdown of STAT3. Moreover, IL-6/sIL-6R partly inhibited TGF-β-induced activation of the Smad-sensitive promoter detected with luciferase reporter gene assays and up-regulation of TGFRI and TGFRII, evaluated by quantitative real-time RT-PCR. Strikingly, overexpression of TGFRI and TGFRII diminished these inhibitory effects of IL-6/sIL-6R. We conclude that of IL-6-mediated trans-signaling potently represses TGF-β signaling in HTM cells.

  15. YAP/TAZ Are Essential for TGF-β2-Mediated Conjunctival Fibrosis. International-journal Peer-reviewed

    Akiko Futakuchi, Toshihiro Inoue, Fan-Yan Wei, Miyuki Inoue-Mochita, Tomokazu Fujimoto, Kazuhito Tomizawa, Hidenobu Tanihara

    Investigative ophthalmology & visual science　59　(7)　3069-3078　2018/06/01

    Publisher: Association for Research in Vision and Ophthalmology Inc.

    DOI： 10.1167/iovs.18-24258 　

    ISSN： 1552-5783 0146-0404

  16. Decreased MCP-1/CCR2 axis-mediated chemotactic effect of conjunctival fibroblasts after transdifferentiation into myofibroblasts. International-journal Peer-reviewed

    Utako Tsutsumi-Kuroda, Toshihiro Inoue, Akiko Futakuchi, Kohei Shobayashi, Eri Takahashi, Sachi Kojima, Miyuki Inoue-Mochita, Tomokazu Fujimoto, Hidenobu Tanihara

    Experimental eye research　170　76-80　2018/05

    Publisher: Academic Press

    DOI： 10.1016/j.exer.2018.02.008 　

    ISSN： 1096-0007 0014-4835

  17. Molecular Mechanisms Underlying the Filtration Bleb-Maintaining Effects of Suberoylanilide Hydroxamic Acid (SAHA). International-journal Peer-reviewed

    Akiko Futakuchi, Toshihiro Inoue, Tomokazu Fujimoto, Utako Kuroda, Miyuki Inoue-Mochita, Eri Takahashi, Saori Ohira, Hidenobu Tanihara

    Investigative ophthalmology & visual science　58　(4)　2421-2429　2017/04/01

    DOI： 10.1167/iovs.16-21403 　

    ISSN： 0146-0404

    eISSN： 1552-5783

  18. The effects of ripasudil (K-115), a Rho kinase inhibitor, on activation of human conjunctival fibroblasts. International-journal Peer-reviewed

    Akiko Futakuchi, Toshihiro Inoue, Tomokazu Fujimoto, Miyuki Inoue-Mochita, Motofumi Kawai, Hidenobu Tanihara

    Experimental eye research　149　107-115　2016/08

    DOI： 10.1016/j.exer.2016.07.001 　

    ISSN： 0014-4835

    eISSN： 1096-0007

  19. Histone deacetylase inhibitor attenuates TGF-beta 2 induced human conjunctival fibroblast activation Peer-reviewed

    Futakuchi Akiko, Inoue Toshihiro, Fujimoto Tomokazu, Kuroda Utako, Inoue Miyuki Mochita, Takahashi Eri, Shobayashi Kohei, Ohira Saori, Kojima Sachi, Tanihara Hidenobu

    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE　56　(7)　2015/06

    ISSN： 0146-0404

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Misc. 17

  1. 基礎研究コラム シグナル情報伝達を担うRNA修飾由来の新しい眼内液性因子

    小川 亜希子, 北澤 耕司, 村上 祐介, 中川 卓

    あたらしい眼科　40　(5)　663-663　2023/05

    Publisher: (株)メディカル葵出版

    ISSN： 0910-1810

  2. 生体恒常性を制御する新しいRNA修飾代謝酵素の機能解明

    小川 亜希子

    日本応用酵素協会誌　(57)　46-47　2023/03

    Publisher: (公財)日本応用酵素協会

    ISSN： 0913-3348

    eISSN： 2434-7914

  3. RNA由来修飾核酸の代謝酵素の同定

    小川 亜希子, 渡部 聡, 稲葉 謙次, 魏 范研

    日本痛風・尿酸核酸学会総会プログラム・抄録集　56回　69-69　2023/01

    Publisher: (一社)日本痛風・尿酸核酸学会

  4. COVID-19ワクチン接種後のRNA修飾代謝物排泄の変動

    小川 亜希子, 松尾 紀孝, 齋藤 一創, 魏 范研

    痛風と尿酸・核酸　46　(2)　105-113　2022/12

    Publisher: (一社)日本痛風・尿酸核酸学会

    eISSN： 2435-0095

  5. RNA修飾由来の新しい核酸型液性因子とその生理的意義について

    小川 亜希子, 魏 范研

    痛風と尿酸・核酸　46　(2)　154-154　2022/12

    Publisher: (一社)日本痛風・尿酸核酸学会

    eISSN： 2435-0095

  6. RNA修飾代謝物のN6-methyladenosine(m6A)は受容体応答を引き起こす新規液性因子である

    小川亜希子, 小川亜希子, 名切千彩恵, 志甫谷渉, 井上飛鳥, 川上耕季, 平塚寿々音, 青木淳賢, 青木淳賢, 伊藤康裕, 鈴木健夫, 鈴木勉, 井上俊洋, 濡木理, 富澤一仁, 魏范研, 魏范研

    日本生化学会大会(Web)　94th　2021

  7. 緑内障薬物治療の未来 続発緑内障に対するリパスジル点眼液の治療効果と適応

    二口 亜希子, 井上 俊洋, 谷原 秀信, ROCK-S研究グループ

    日本緑内障学会抄録集　30回　53-53　2019/09

    Publisher: 日本緑内障学会

  8. 結膜下組織瘢痕化におけるIL-6ファミリーの影響について

    渡邊 文香, 二口 亜希子, 藤本 智和, 井上 みゆき, 井上 俊洋

    日本緑内障学会抄録集　30回　190-190　2019/09

    Publisher: 日本緑内障学会

  9. Summing Up 緑内障の病態

    二口 亜希子, 井上 俊洋

    Frontiers in Glaucoma　(57)　34-43　2019/03

    Publisher: (株)メディカルレビュー社

    ISSN： 1345-854X

  10. マウス結膜生体イメージングによるK115のMCP-1誘発炎症抑制効果の検証

    小島 祥, 船蔵 直史, 川畑 和幸, 藤本 智和, 二口 亜希子, 谷原 秀信, 井上 俊洋

    日本眼科学会雑誌　123　(臨増)　241-241　2019/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  11. ヒト結膜線維芽細胞の筋線維芽細胞への分化に対するDNAメチル基転移酵素阻害剤の影響

    米村 瞳, 井上 俊洋, 井上 みゆき, 二口 亜希子, 藤本 智和, 堤 詩子, 谷原 秀信

    日本眼科学会雑誌　122　(臨増)　165-165　2018/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  12. Hippoシグナルのエフェクター、YAP/TAZがヒト結膜線維化モデルに及ぼす影響

    二口 亜希子, 井上 俊洋, 井上 みゆき, 藤本 智和, 谷原 秀信

    生命科学系学会合同年次大会　2017年度　[2P-0440]　2017/12

    Publisher: 生命科学系学会合同年次大会運営事務局

  13. ボリノスタット(SAHA)が結膜線維芽細胞に及ぼす影響

    二口 亜希子, 井上 俊洋, 藤本 智和, 黒田 詩子, 高橋 枝里, 井上 みゆき, 谷原 秀信

    日本眼科学会雑誌　121　(臨増)　184-184　2017/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  14. ヒト結膜線維芽細胞および筋線維芽細胞のMCP-1分泌と、単球系細胞遊走への影響

    堤 詩子, 井上 俊洋, 正林 耕平, 二口 亜希子, 高橋 枝里, 小島 祥, 井上 みゆき, 藤本 智和, 谷原 秀信

    日本眼科学会雑誌　121　(臨増)　317-317　2017/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  15. 緑内障手術のサイエンス 濾過手術とサイトカインを中心に

    井上 俊洋, 谷原 秀信, 布田 龍佑, 福島 美紀子, 伊藤 康裕, 川路 隆博, 岩尾 圭一郎, 高橋 枝里, 藤本 智和, 井上 みゆき, 岩尾 美奈子, 笠岡 奈々子, 原 竜平, 正林 耕平, 榮木 大輔, 大平 さおり, 後藤 章子, 小島 祥, 芳賀 彰, 黒田 詩子, 中島 圭一, 平川 沙織, 福島 亜矢子, 松村 理世, 徳永 瞳, 川畑 和幸, 北村 文香, 西澤 麻保, 二口 亜希子, 松本 桃佳, 吉村 長久, 亀田 隆範, 吉田 晃敏, 川井 基史, 川井 尚子, 木下 茂, 上田 真由美, 古賀 彩加, 稲谷 大, 瀧原 祐史, 本庄 恵, 石井 優, 菊田 順一, 古家 雅之, 松川 昭博, 猿渡 淳二, 田賀 哲也, 鹿川 哲史

    日本眼科学会雑誌　121　(3)　314-335　2017/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

  16. Histone deacetylase阻害剤がヒト結膜創傷治癒モデルに及ぼす影響の網羅的遺伝子解析

    二口 亜希子, 井上 俊洋, 藤本 智和, 黒田 詩子, 井上 みゆき, 正林 耕平, 大平 さおり, 小島 祥, 谷原 秀信

    日本緑内障学会抄録集　26回　116-116　2015/09

    Publisher: 日本緑内障学会

  17. ヒト結膜線維芽細胞の活性化に対するHDAC阻害剤の効果

    二口 亜希子, 井上 俊洋, 藤本 智和, 黒田 詩子, 井上 みゆき, 高橋 枝里, 正林 耕平, 大平 さおり, 小島 祥, 谷原 秀信

    日本眼科学会雑誌　119　(臨増)　220-220　2015/03

    Publisher: (公財)日本眼科学会

    ISSN： 0029-0203

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Books and Other Publications 5

  1. 修飾RNAによる免疫制御リガンドとしての作用

    小川亜希子, 魏范研

    公益社団法人 日本生化学会 「生化学」95巻5号　2023/10

  2. シグナル情報伝達を担うRNA由来液性因子

    医歯薬出版「医学のあゆみ」　2022/01

  3. RNA修飾の生理機能

    ニュー・サイエンス社 「細胞」 特集「エピトランスクリプトーム」　2021/12

  4. 緑内障の病態

    メディカルレビュー社 Frontiers in Glaucoma　2019

  5. 特集 大事な特徴がわかる! 患者さんの心に響く説明ができる! 緑内障点眼薬スペシャルノート. 6 交感神経α2刺激薬 7 Rhoキナーゼ阻害薬

    メディカ出版 眼科ケア　2017

Presentations 22

  1. Regulatory roles of RNA modifications in glaucoma pathophysiology

    Akiko Ogawa

    16th Europe Glaucoma Congress　2024/06

  2. Metabolic regulation of modified RNA in physiology and pathology

    Akiko Ogawa

    RNA Society Annual Meeting 2024　2024/05

  3. COVID19治療薬レムデシビルの 副作用の機序解明

    小川亜希子

    第57回日本痛風・尿酸核酸学会総会　2024/03

  4. Modified adenosine metabolism safeguards energy balance

    2024/03

  5. RNA修飾とその代謝シグナルが開拓する 生体の病態生理学

    小川亜希子

    第46回日本分子生物学会年会　2023/12

  6. 続発緑内障に対する リパスジル点眼液の治療効果と適応 Invited

    小川亜希子

    第7回アリエスの会　2023/11

  7. リパスジル(K115)の緑内障病態における ミトコンドリア特異的RNA修飾に対する機能 Invited

    小川亜希子

    第9回Japan ROCK Conference　2023/11

  8. 修飾RNAの分解産物による オートファジー経路の解明に向けて

    小川亜希子

    第5回「マルチモードオートファジー」班会議 第15回オートファジー研究会　2023/11

  9. Investigation of the regulatory mechanism of homeostasis through the metabolism of RNA modification Invited

    2023/10

  10. COVID19治療薬レムデシビルは ウロテンシン受容体を活性化することで 心筋細胞の機能不全を引き起こす

    小川亜希子

    第96回生化学会大会　2023/10

  11. 緑内障病態における ミトコンドリア特異的RNA修飾の機能

    小川亜希子

    第34回日本緑内障学会 学会長企画 「新進気鋭の緑内障研究者の競演」　2023/09

  12. Extracellular modified nucleosides derived from RNA catabolism activates GPCR Invited

    2023/09

  13. Novel RNA modification signaling and its implication in glaucoma pathophysiology

    Akiko Ogawa

    10th World Glaucoma Congress　2023/07

  14. シグナル情報伝達を担う RNA修飾由来の液性因子 Invited

    小川亜希子

    第11回タタバイオ分子クラブ　2023/07

  15. Modified adenosine metabolism safeguards energy balance

    小川亜希子

    第24回日本RNA学会　2023/07

  16. Metabolic regulation of modified RNA in immunity and disease

    2023/06

  17. Extracellular modified nucleosides derived from RNA catabolism activates GPCR

    Akiko Ogawa

    RNA Society Annual Meeting 2023　2023/05

  18. RNA由来修飾核酸の代謝酵素の同定

    小川亜希子

    第56回 日本痛風・尿酸核酸学会総会 優秀演題賞候補セッション　2023/02

  19. RNAモドミクスが開拓する 新しい眼内病態生理学 Invited

    小川亜希子

    第126回日本眼科学会総会 シンポジウム　2022/04/14

  20. 濾過手術後の創傷治癒抑制薬物治療の可能性 Invited

    第31回日本緑内障学会 シンポジウム　2020/10/03

  21. 続発緑内障に対するリパスジル点眼液の治療効果と適応. Invited

    第30回日本緑内障学会 シンポジウム　2019

  22. 緑内障術後の線維（瘢痕）化を制御する新たな治療開発に関する研究. Invited

    第29回 日本緑内障学会 シンポジウム　2018

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Research Projects 8

  1. 修飾RNA代謝を基軸とする生体恒常性ネットワークの解明

    小川 亜希子

    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

    2024/02/28 - 2026/03/31

  2. Molecular basis of RNA modification in immune response after transplantation and cell therapy and novel biomarkers

    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

    2023/04/01 - 2026/03/31

  3. A synthetic metabolic network based on RNA modification for biological homeostasis

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

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

    Institution: Tohoku University

    2022/04/01 - 2026/03/31

  4. 次世代RNA医薬の基盤創生への挑戦

    小川 亜希子

    Offer Organization: 日本学術振興会

    System: 科学研究費助成事業

    Category: 挑戦的研究(萌芽)

    Institution: 東北大学

    2023/06/30 - 2025/03/31

  5. RNAモドミクスを基軸とする新規核酸生理学の開拓

    魏 范研, 小川 亜希子, 松田 盛

    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

    2021/04/01 - 2025/03/31

  6. Investigation of the mechanism of autophagy pathway by novel metabolites derived from modified RNA.

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)

    Institution: Tohoku University

    2022/04/01 - 2024/03/31

  7. Modulation of mitochondrial function by reactive sulfur signaling

    Wei Fan-Yan

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

    Category: Grant-in-Aid for Challenging Research (Exploratory)

    Institution: Tohoku University

    2020/07/30 - 2022/03/31

    More details Close

    Mitochondrial disease is a rare genetic disease characterized by the catastrophic impairment of mitochondrial metabolism caused by pathogenic mutations in mitochondrial DNA or nuclear DNA. However, there is no effective treatment for mitochondrial disease. Recently, our research has discovered that the reactive sulfur species-mediated signaling is involved in the pathogenesis of mitochondrial disease. We found that the reactive sulfur species donate sulfur atoms to mitochondrial tRNA to form tRNA thiolation. Decrease of mitochondrial tRNA thiolation is responsible for the alteration of mitochondrial protein translation and the subsequent metabolic dysfunction. In the current study, we performed a comprehensive genetic screening using shRNA library targeting genes that are related to mitochondrial functions. We identified that knockdown of several genes can lead to the recovery of mitochondrial membrane potential and cell growth in a mitochondrial disease cell model.

  8. The emerging role of RNA modifications in the regulation of glaucoma pathology

    Ogawa Akiko

    Offer Organization: Japan Society for the Promotion of Science

    System: Grants-in-Aid for Scientific Research

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

    Institution: Tohoku University

    2020/04 - 2022/03

    More details Close

    This study presents biochemical and structural evidence that extracellular m6A is generated from modified-RNA catabolism and is a potent and selective ligand of adenosine A3 receptor. This study provides a framework for understanding the roles played by the complex pantheon of extracellular modified nucleosides.

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Media Coverage 4

  1. 「アイフレイル」の進行を防ぎたい 核酸研究を治療や予防に応用

    JST　JSTnews【さきがける科学人】（JST広報誌）

    2023/09

    Type: Newspaper, magazine

  2. COVID-19治療薬副作用の仕組み解明

    東北大学　東北大学新聞

    2023/07

    Type: Newspaper, magazine

  3. 東北大学など、新型コロナ治療薬 副作用の仕組みを解明

    日本経済新聞　日本経済新聞 電子版

    2023/05

    Type: Internet

  4. COVID-19 治療薬の副作用の仕組みを解明 -受容体経路を抑制する ことで副作用改善の可能性-

    東北大学　東北大学プレスリリース

    2023/05

    Type: Internet