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Inductions of granulosa cell luteinization and cumulus expansion are dependent on the fibronectin-integrin pathway during ovulation process in mice

https://hiroshima.repo.nii.ac.jp/records/2007971
https://hiroshima.repo.nii.ac.jp/records/2007971
03785e1a-1c5c-42cd-9bee-d60a0e095101
名前 / ファイル ライセンス アクション
PLoSONE_13_e0192458.pdf PLoSONE_13_e0192458.pdf (20.7 MB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Inductions of granulosa cell luteinization and cumulus expansion are dependent on the fibronectin-integrin pathway during ovulation process in mice
言語 en
作成者 Kitasaka, Hiroya

× Kitasaka, Hiroya

en Kitasaka, Hiroya

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Kawai, Tomoko

× Kawai, Tomoko

en Kawai, Tomoko

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Hoque, S. A. Masudul

× Hoque, S. A. Masudul

en Hoque, S. A. Masudul

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Umehara, Takashi

× Umehara, Takashi

en Umehara, Takashi

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Fujita, Youko

× Fujita, Youko

en Fujita, Youko

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Shimada, Masayuki

× Shimada, Masayuki

en Shimada, Masayuki

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 © 2018 Kitasaka et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
内容記述
内容記述 It has been known that EGF-like factor secreted from LH-stimulated granuloma cells acts on granulosa cells and cumulus cells to induce ovulation process. Granulosa cells are changed the morphology with differentiating cell functions to produce progesterone. Cumulus cells are detached to make a space between the cells to accumulate hyaluronan rich matrix. LH also changes extracellular matrix (ECM) components including fibronectin in the follicular walls and granulosa cell layers. EGF like factor and fibronectin synergistically play important roles in numerous cell functions, especially cancer cell migration, estimating that fibronectin would impact on granulosa cells and cumulus cells. To clear this hypothesis, the localizations of fibronectin and its receptor integrin were observed by immunofluorescence technique. The functions were monitored by the detection of downstream signaling pathway, focal adhesion kinase (FAK). The pharmacological approach in both in vivo and in vitro were used for analyzing the physiological roles of FAK during ovulation process. The immunofluorescence staining revealed that fibronectin and integrin were observed in granulosa cells, cumulus cells and the space between cumulus cells and oocyte at 4 and 8 h after hCG injection. Concomitantly with the changes of fibronectin-integrin localization, FAK was phosphorylated in periovulatory follicles. The injection of FAK inhibitor suppressed not only ovulation but also luteinization of granulosa cells and cumulus expansion. In cultured-granulosa cells, fibronectin-integrin synergistically activated FAK with amphiregulin (AREG). Such cooperative stimulations induced a morphological change in granulosa cells, which resulted in the maximum level of progesterone production via the induction of Hsd3b. When cumulus-oocyte complexes (COCs) were cultured with AREG in the presence of serum, the maximum level of cumulus expansion was observed. The AREG-induced cumulus expansion was also suppressed by FAK inhibitor. Thus, it is concluded that fibronectin and AREG synergistically activate FAK not only in granulosa cells and cumulus cells to induce successful ovulation process.
言語 en
内容記述
内容記述タイプ Other
内容記述 This work was supported in part by JSPS KAKENHI Grant Number JP24688028 and JP 16H05017 (to M.S.) and the Japan Agency for Medical Research and Development (AMED) 16gk0110015h0001 (to M.S.).
出版者
出版者 Public Library of Science
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
関連情報
識別子タイプ DOI
関連識別子 10.1371/journal.pone.0192458
関連情報
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.pone.0192458
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1932-6203
開始ページ
開始ページ e0192458
書誌情報 PLoS ONE
PLoS ONE

巻 13, 号 2, p. e0192458, 発行日 2018-02-08
旧ID 48664
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