Affiliation |
Faculty of Medicine School of Medicine Department of Medical Sciences, Pharmacology |
Title |
Assistant Professor |
External Link |
MIURA Ayako
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Research Areas 【 display / non-display 】
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Life Science / Respiratory medicine
Papers 【 display / non-display 】
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The NERP-4–SNAT2 axis regulates pancreatic β-cell maintenance and function Reviewed International coauthorship
Weidong Zhang, Ayako Miura, Md Moin Abu Saleh, Koichiro Shimizu, Yuichiro Mita, Ryota Tanida, Satoshi Hirako, Seiji Shioda, ValeryGmyr, Julie Kerr-Conte, Francois Pattou,Chunhuan Jin, Yoshikatsu Kanai, Kazuki Sasaki, Naoto Minamino, Hideyuki Sakoda & Masamitsu Nakazato
Nature Communications 14 ( 8158 ) 2023.12
Authorship:Lead author Language:English Publishing type:Research paper (scientific journal)
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Maruta T., Kouroki S., Kurogi M., Hidaka K., Koshida T., Miura A., Nakagawa H., Yanagita T., Takeya R., Tsuneyoshi I.
Journal of Neuroscience Research 102 ( 10 ) 2024.10
Publishing type:Research paper (scientific journal) Publisher:Journal of Neuroscience Research
Voltage-gated sodium channels, including NaV1.7, NaV1.8, and NaV1.9, play important roles in pain transmission and chronic pain development. However, the specific mechanisms of their action remain unclear, highlighting the need for in vivo stimulation studies of these channels. Optogenetics, a novel technique for targeting the activation or inhibition of specific neural circuits using light, offers a promising solution. In our previous study, we used optogenetics to selectively excite NaV1.7-expressing neurons in the dorsal root ganglion of mice to induce nocifensive behavior. Here, we further characterize the impact of nocifensive behavior by activation of NaV1.7, NaV1.8, or NaV1.9-expressing neurons. Using CRISPR/Cas9-mediated homologous recombination, NaV1.7–iCre, NaV1.8–iCre, or NaV1.9–iCre mice expressing iCre recombinase under the control of the endogenous NaV1.7, NaV1.8, or NaV1.9 gene promoter were produced. These mice were then bred with channelrhodopsin-2 (ChR2) Cre–reporter Ai32 mice to obtain NaV1.7–ChR2, NaV1.8–ChR2, or NaV1.9–ChR2 mice. Blue light exposure triggered paw withdrawal in all mice, with the strongest response in NaV1.8–ChR2 mice. These light sensitivity differences observed across NaV1.x–ChR2 mice may be dependent on ChR2 expression or reflect the inherent disparities in their pain transmission roles. In conclusion, we have generated noninvasive pain models, with optically activated peripheral nociceptors. We believe that studies using optogenetics will further elucidate the role of sodium channel subtypes in pain transmission.
DOI: 10.1002/jnr.25386
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The expression of the formin Fhod3 in mouse tongue striated muscle Reviewed International coauthorship
Nakagawa Hikaru, Kage Yohko, Miura Ayako, Sulistomo Hikmawan Wahyu, Matsuyama Sho, Yamashita Yoshihiro, Takeya Ryu
Cell Structure and Function advpub ( 0 ) 2024
Language:English Publishing type:Research paper (scientific journal) Publisher:日本細胞生物学会
The sarcomere is the contractile unit of striated muscle and is composed of actin and myosin filaments. There is increasing evidence to support that actin assembly mediated by Fhod3, a member of the formin family of proteins, is critical for sarcomere formation and maintenance in cardiac muscle. Fhod3, which is abundantly expressed in the heart, localizes to the center of sarcomeres and contributes to the regulation of the cardiac function, as evidenced by the fact that mutations in Fhod3 cause cardiomyopathy. However, the role of Fhod3 in skeletal muscle, another type of striated muscle, is unclear. We herein show that Fhod3 is expressed in the tongue at both mRNA and protein levels, although in smaller amounts than in the heart. To determine the physiological role of Fhod3 expressed in the tongue, we generated embryos lacking Fhod3 in the tongue. The tongue tissue of the Fhod3-depleted embryos did not show any significant structural defects, suggesting that Fhod3 is dispensable for normal development of the mouse tongue. Unexpectedly, the immunostaining analysis revealed the absence of specific sarcomeric signals for Fhod3 in the wild-type tongue when compared to the Fhod3-depleted tongue as a negative control, despite the use of antibodies that had previously been validated by immunostaining of heart tissues. Taken together, although Fhod3 protein is expressed at a significant level in the tongue, Fhod3 in the tongue does not appear to exhibit the same sarcomeric pattern as observed in the heart, suggesting a different role for Fhod3 in the tongue muscles.Key words: actin, formin, sarcomere, striated muscle
DOI: 10.1247/csf.24044
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The NERP-4–SNAT2 axis regulates pancreatic β-cell maintenance and function Reviewed
Zhang W., Miura A., Abu Saleh M.M., Shimizu K., Mita Y., Tanida R., Hirako S., Shioda S., Gmyr V., Kerr-Conte J., Pattou F., Jin C., Kanai Y., Sasaki K., Minamino N., Sakoda H., Nakazato M.
Nature Communications 14 ( 1 ) 2023.12
Publishing type:Research paper (scientific journal) Publisher:Nature Communications
Insulin secretion from pancreatic β cells is regulated by multiple stimuli, including nutrients, hormones, neuronal inputs, and local signalling. Amino acids modulate insulin secretion via amino acid transporters expressed on β cells. The granin protein VGF has dual roles in β cells: regulating secretory granule formation and functioning as a multiple peptide precursor. A VGF-derived peptide, neuroendocrine regulatory peptide-4 (NERP-4), increases Ca2+ influx in the pancreata of transgenic mice expressing apoaequorin, a Ca2+-induced bioluminescent protein complex. NERP-4 enhances glucose-stimulated insulin secretion from isolated human and mouse islets and β-cell–derived MIN6-K8 cells. NERP-4 administration reverses the impairment of β-cell maintenance and function in db/db mice by enhancing mitochondrial function and reducing metabolic stress. NERP-4 acts on sodium-coupled neutral amino acid transporter 2 (SNAT2), thereby increasing glutamine, alanine, and proline uptake into β cells and stimulating insulin secretion. SNAT2 deletion and inhibition abolish the protective effects of NERP-4 on β-cell maintenance. These findings demonstrate a novel autocrine mechanism of β-cell maintenance and function that is mediated by the peptide–amino acid transporter axis.
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Matsuo A, Tanida R, Yanagi S, Tsubouchi H, Miura A, Shigekusa T, Matsumoto N, Nakazato M
European journal of pharmacology 892 173754 2021.2
Language:Japanese Publishing type:Research paper (scientific journal) Publisher:European Journal of Pharmacology
© 2020 The Authors Fibrotic scarring is an important prognostic factor of acute respiratory distress syndrome (ARDS). There are currently no antifibrotic drugs or other therapeutic agents for ARDS. Lysyl oxidase-like 2 (LOXL2), an amine oxidase, contributes to fibrotic scarring by facilitating collagen cross-linking. Recent clinical trials revealed that a monoclonal inhibitory antibody against LOXL2 failed to show benefit over placebo in patients with fibrotic disorders involving the lungs. These clinical results raise the possibility that targeting the extracellular enzymic activity of LOXL2 is not in itself sufficient to prevent fibrotic scarring. We investigated the role of LOXL2 in the pathogenesis of ARDS in vivo, in vitro, and in samples from patients with ARDS. After lung injury, LOXL2 was unevenly expressed in the nuclei of lung fibroblasts and myofibroblasts in the fibrotic phase. Nuclear LOXL2 expression was upregulated in lung fibroblasts after transforming growth factor-beta1 (TGF-β1)-treatment. LOXL2 silencing abrogated the TGF-β1-induced expression of a myofibrogenic-progenitor marker, the appearance of proto-myofibroblasts, and the evolution of differentiated myofibroblasts in lung fibroblasts. Nuclear upregulation of Snail was evident in myofibroblasts during the fibrotic phase after lung injury. We detected high levels of LOXL2 protein in the lungs of ARDS patients, specifically during the proliferative and fibrotic phases. Our results highlight nuclear LOXL2 in fibroblasts as a primary causative driver of cell-fate decision toward myofibroblasts and of the progression of fibrotic scarring. A nuclear-LOXL2-targeted agent could be a promising therapeutic strategy against fibrotic disorders including ARDS.
Presentations 【 display / non-display 】
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Role of ERM proteins in the regulation of actin cytoskeleton in migrating alveolar macrophage
Ayako Miura,Fumiyuki Sanematsu,Ryu Takeya
2023.12
Event date: 2023.12.14 - 2023.12.16
Language:English Presentation type:Poster presentation
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Regulation of directional cell motility in alveolar macrophages by a formin family protein Fhod1
Ayako Miura,Fumiyuki Sanematsu,Ryu Takeya
2022.11
Event date: 2022.11.30 - 2022.12.3
Language:English Presentation type:Poster presentation
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ARDS線維化過程におけるfibroblast/myofibroblastの核内LOXL2阻害の意義
松尾彩子、谷田亮太、柳 重久、坪内拡伸、三浦綾子、重草貴文、松元信弘、中里雅光、宮崎泰可
第62回日本呼吸器学会学術講演会 2022.4
Event date: 2022.4.22 - 2022.4.24
Language:Japanese Presentation type:Oral presentation (general)
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The actin-nucleating protein Fhod1 in alveolar macrophage
Ayako Miura,Fumiyuki Sanamatsu,Ryu Takeya
2022.3
Event date: 2022.3.7 - 2022.3.9
Language:English Presentation type:Poster presentation
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NMU induces β cell failure by triggering mitochondrial dysfunction and ER stress
張維東、迫田秀之、三浦綾子、中里雅光
AMED-CREST International Symposium. Miyazaki.
Event date: 2020.1.31 - 2020.2.2
Language:English Presentation type:Poster presentation
Awards 【 display / non-display 】
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ERS Young Scientist Sponsorship
2016.9 Europian Respiratory Society The role of Pten in the cell-fate determination of epithelial cells in lung development.
三浦綾子
Award type:Award from international society, conference, symposium, etc. Country:United Kingdom
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Kyushu Diabetes Research Conference 最優秀奨励賞
2016.7 Kyusyu Diabetes Research Conference 糖代謝調節に機能する新規生理活性ペプチドの発見
三浦綾子
Award type:Award from Japanese society, conference, symposium, etc. Country:Japan
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児玉記念基礎医学助成基金 優秀研究論文顕彰
2013.10 児玉記念基礎医学助成基金 Pituitary adenylate cyclase-activating polypeptide type 1 receptor (PAC1) gene is suppressed by transglutaminase 2 activation.
三浦綾子
Award type:Award from publisher, newspaper, foundation, etc. Country:Japan
Grant-in-Aid for Scientific Research 【 display / non-display 】
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異種細胞間の細胞接着装置の恒常性維持機構の解析
Grant number:21K08183 2021.04 - 2024.03
独立行政法人日本学術振興会 科学研究費補助金 基盤研究(C)
Authorship:Principal investigator
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サルコメアは回転トルクを生み出すか?
Grant number:22K19407 2022.04 - 2024.03
独立行政法人日本学術振興会 科学研究費補助金 挑戦的研究(萌芽)
武谷 立、
Authorship:Coinvestigator(s)
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The Role of Epithelial Pten in Epithelial Cell Fate and Programmed Cellular Senescence during Lung Development
Grant number:17K16051 2017.04 - 2021.03
Grant-in-Aid for Scientific Research Grant-in-Aid for Young Scientists(B)
Authorship:Principal investigator
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上皮間葉連関を焦点とした肺発生での上皮Ptenの機能解析
Grant number:26860610 2014.04 - 2016.03
科学研究費補助金 若手研究(B)
Authorship:Principal investigator