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ID 47119
本文ファイル
著者
Hirose, Kentaro
Shiomi, Taishi
Hozumi, Shunya 大学院理学研究科 広大研究者総覧
Kikuchi, Yutaka 大学院理学研究科 広大研究者総覧
キーワード
Mechanistic target of rapamycin
Fin
Regeneration
Zebrafish
Osteoblast
Cell proliferation
Cell survival
Differentiation
NDC
生物科学・一般生物学
抄録(英)
[Background]:The mechanistic target of rapamycin complex1 (mTORC1) signaling pathway has been implicated in functions of multicellular processes, including cell growth and metabolism. Although recent reports showed that many signaling pathways, including Activin, Bmp, Fgf, sonic hedgehog, Insulin-like growth factor (IGF), Notch, retinoic acid, and Wnt, are implicated in non-mammalian vertebrate regeneration, also known as epimorphic regeneration, mTORC1 function remains unknown.
[Results]:To investigate the role of mTORC1 signaling pathway in zebrafish caudal fin, we examined the activation and function of mTORC1 signaling using an antibody against phosphorylated S6 kinase and a specific inhibitor, rapamycin. mTORC1 signaling is activated in proliferative cells of intra-ray and wound epidermal cells before blastema formation, as well as in proliferative blastema cells, wound epidermal cells, and osteoblasts during regenerative outgrowth. Before blastema formation, proliferation of intra-ray and wound epidermal cells is suppressed, but cell death is not affected by mTORC1 signaling inhibition with rapamycin. Moreover, rapamycin treatment inhibits blastema and wound epidermal cell proliferation and survival during blastema formation and regenerative outgrowth, as well as osteoblast proliferation and differentiation during regenerative outgrowth. We further determined that mTORC1 signaling is regulated through IGF-1 receptor/phosphatidylinositol-3 kinase and Wnt pathways during fin regeneration.
[Conclusion]:Taken together, our findings reveal that mTORC1 signaling regulates proliferation, survival, and differentiation of intra-ray cells, wound epidermis, blastema cells, and/or osteoblasts in various fin regeneration stages downstream of IGF and Wnt signaling pathways.
内容記述
This study was supported by grants from Grant-in-Aid for Scientific Research from the JSPS (KAKENHI 23616002) to Y.K., and from Hiroshima University Alumni Association Research Grant & Hiroshima University Support Foundation Research and Grant-in-Aid for Scientific Research from the JSPS (KAKENHI 26 · 6771) to K.H.
掲載誌名
BMC Developmental Biology
14巻
開始ページ
42
出版年月日
2014-12-06
出版者
BioMed Central
ISSN
1471-213X
出版者DOI
PubMedID
言語
英語
NII資源タイプ
学術雑誌論文
広大資料タイプ
学術雑誌論文
DCMIタイプ
text
フォーマット
application/pdf
著者版フラグ
publisher
権利情報
© 2014 Hirose et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
関連情報URL
部局名
理学研究科