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Affiliation |
Faculty of Medicine School of Medicine Department of Medical Sciences, Pharmacology |
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Assistant Professor |
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Related SDGs |
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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NERP-4–Deleted VGF Impairs β-Cell Granulogenesis and Insulin Secretion Reviewed
Zhang W., Nakazato Y., Minamino N., Okumura N., Miura A., Tarusawa T., Mizukami H., Sakoda H., Nakazato M.
FASEB Journal 39 ( 24 ) 2025.12
Language:English Publishing type:Research paper (scientific journal) Publisher:FASEB Journal
Neuroendocrine regulatory peptide-4 (NERP-4) processed from the granin protein VGF functions as a positive allosteric modulator that acts on the amino acid transporter SNAT2 expressed on pancreatic β cells. NERP-4 promotes insulin secretion and β-cell maintenance. We studied the effects of NERP-4–deleted VGF (VGF<sup>△NERP-4</sup>) on β-cell functions in MIN6-K8 β cells and CRISPR-Cas9–designed mouse islets. VGF<sup>△NERP-4</sup> exhibited reduced insulin secretion and disrupted β-cell maintenance. Notably, VGF<sup>△NERP-4</sup> caused defective insulin granule formation via insulin accumulation in the trans-Golgi network, thereby reducing replenishment of insulin granule stores in the second-phase insulin secretion. These findings are comparable to those obtained in Vgf knockdown. NERP-4 administration to VGF<sup>△NERP-4</sup> β cells restored β-cell maintenance but not insulin granule formation. NERP-4 was reduced in the islets of patients with type 2 diabetes mellitus. NERP-4 plays a role in β-cell viability and the NERP-4 region is critical for VGF structure in the context of granulogenesis, thereby providing new insights into the role of NERP-4 in β-cell biology.
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丸田 豊明, 日髙 康太郎, 越田 智広, 黒木 未央, 鹿毛 陽子, 三浦 綾子, 中川 光, 柳田 俊彦, 武谷 立, 恒吉 勇男
Plos One 20 ( 5 ) e0323628 2025.5
Language:English Publishing type:Research paper (scientific journal) Publisher:Public Library of Science (PLoS)
Neuropathic pain has a significant social impact, with high morbidity and reduced productivity, the underlying mechanisms of neuropathic pain remain poorly understood, and effective therapeutic strategies remain elusive. The development of animal models of neuropathic pain that stimulate only the nociceptors and not the other sensory receptors or motor nerves is desirable for elucidating the complex pathogenesis of neuropathic pain. We have previously reported the generation of NaV1.7−channelrhodopsin-2 (ChR2), NaV1.8−ChR2, and NaV1.9−ChR2 mice. Optogenetics was employed in these light-responsive pain mice for generating nociceptive pain by specifically exciting the spinal dorsal root ganglion neurons, in which the respective Na+ channels are expressed through exposure to blue light. This study aimed to compare the neuropathic pain produced by the prolonged exposure of light-responsive pain mice to blue light. A reversible neuropathic pain state was established persisting for a minimum of 24 hours when each light-responsive pain mouse was irradiated with light of an intensity that consistently elicited pain. Furthermore, the mice also showed pain sensitivity to light irradiation and mechanical stimulation. The expression of c-Fos, a marker for neuronal activity following noxious stimulation, was increased in the dorsal horn of the spinal cord on the light irradiated side. DS-1971a, a selective NaV1.7 inhibitor, was effective in attenuating neuropathic pain in all light-responsive pain mice. In conclusion, optogenetics helps elucidate the specific functions of sodium channel subtypes in pain signaling, thereby advancing our understanding and paving the way for the development of further effective treatments for pain disorders in the future.
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Kouroki S., Maruta T., Hidaka K., Koshida T., Kurogi M., Kage Y., Miura A., Nakagawa H., Yanagita T., Takeya R., Tsuneyoshi I.
Plos One 20 ( 5 May ) 2025.5
Publishing type:Research paper (scientific journal) Publisher:Plos One
Neuropathic pain has a significant social impact, with high morbidity and reduced productivity, the underlying mechanisms of neuropathic pain remain poorly understood, and effective therapeutic strategies remain elusive. The development of animal models of neuropathic pain that stimulate only the nociceptors and not the other sensory receptors or motor nerves is desirable for elucidating the complex pathogenesis of neuropathic pain. We have previously reported the generation of Na<inf>V</inf>1.7−channelrhodopsin-2 (ChR2), Na<inf>V</inf>1.8−ChR2, and Na<inf>V</inf>1.9−ChR2 mice. Optogenetics was employed in these light-responsive pain mice for generating nociceptive pain by specifically exciting the spinal dorsal root ganglion neurons, in which the respective Na<sup>+</sup> channels are expressed through exposure to blue light. This study aimed to compare the neuropathic pain produced by the prolonged exposure of light-responsive pain mice to blue light. A reversible neuropathic pain state was established persisting for a minimum of 24 hours when each light-responsive pain mouse was irradiated with light of an intensity that consistently elicited pain. Furthermore, the mice also showed pain sensitivity to light irradiation and mechanical stimulation. The expression of c-Fos, a marker for neuronal activity following noxious stimulation, was increased in the dorsal horn of the spinal cord on the light irradiated side. DS-1971a, a selective Na<inf>V</inf>1.7 inhibitor, was effective in attenuating neuropathic pain in all light-responsive pain mice. In conclusion, optogenetics helps elucidate the specific functions of sodium channel subtypes in pain signaling, thereby advancing our understanding and paving the way for the development of further effective treatments for pain disorders in the future.
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Reversible neuropathic pain model created by long-term optogenetic nociceptor stimulation using light-responsive pain mice Reviewed
Satoshi Kouroki, Toyoaki Maruta, Kotaro Hidaka, Tomohiro Koshida, Mio Kurogi, Yohko Kage, Ayako Miura, Hikaru Nakagawa, Toshihiko Yanagita, Ryu Takeya, Isao Tsuneyoshi
PLOS ONE 2025.4
Language:English Publishing type:Research paper (scientific journal)
Books 【 display / non-display 】
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PACAP・VIP受容体の構造と機能の多様性 -PACAPの中枢神経機能を中心として-
宮田篤郎, 三浦綾子( Role: Joint author)
医学のあゆみ. 医歯薬出版. 第五土曜特集. 2010;233(9),928-33. 2010
Language:Japanese Book type:Scholarly book
Presentations 【 display / non-display 】
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遊走する肺胞マクロファージの前後極性の維持におけるアクチン核化重合因子の役割
三浦綾子、實松史幸、武谷立
第78回日本薬理学会西南部会 2025.11.8
Event date: 2025.11.8
Language:Japanese Presentation type:Oral presentation (general)
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新規ペプチドNERP-4はアミノ酸トランスポーターSNAT2を介して膵β細胞機能を改善する International coauthorship
三浦 綾子、張 維東、迫田 秀之、南野 直人、中里 雅光
第77回日本薬理学会西南部会 2024.11.16
Event date: 2024.11.16
Language:Japanese Presentation type:Oral presentation (general)
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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)
Awards 【 display / non-display 】
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松尾壽之賞
2025.3 宮崎大学 ペプチド研究を基盤とした生体機能制御機構の解析
三浦綾子
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肺がん検診への導入を目指した診断技術の開発に関する臨床疫学研究
2018 2018年度がん研究財団シニアリサーチフェロー
三浦綾子
Award type:Award from Japanese society, conference, symposium, etc.
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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
Social Activities 【 display / non-display 】
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令和5年度宮崎サイエンスキャンプ「“くすり”は何故効くの?」
Role(s): Lecturer, Organizing member
2023.8.7 - 2023.8.8
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日南学園高等学校田野看護専攻科「生物学」講義
Role(s): Lecturer
2020.6.11 - Now
Audience: High school students
Type:Other