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Endothelial PI3K-C2α, a class II PI3K, has an essential role in angiogenesis and vascular barrier function
http://hdl.handle.net/2297/32825
http://hdl.handle.net/2297/328258b6f2eee-ac4d-4654-8156-9aabd6daf9af
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-YOSHIOKA-K-1560.pdf (1.9 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | Endothelial PI3K-C2α, a class II PI3K, has an essential role in angiogenesis and vascular barrier function | |||||
| 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 | |||||
| 著者 |
Yoshioka, Kazuaki
× Yoshioka, Kazuaki× Yoshida, Kotaro× Cui, Hong× Wakayama, Tomohiko× Takuwa, Noriko× Okamoto, Yasuo× Du, Wa× Qi, Xun× Asanuma, Ken× Sugihara, Kazushi× Aki, Sho× Miyazawa, Hidekazu× Biswas, Kuntal× Nagakura, Chisa× Ueno, Masaya× Iseki, Shoichi× Schwartz, Robert J.× Okamoto, Hiroshi× Sasaki, Takehiko× Matsui, Osamu× Asano, Masahide× Adams, Ralf H.× Takakura, Nobuyuki× Takuwa, Yoh |
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| 書誌情報 |
Nature Medicine 巻 18, 号 10, p. 1560-1569, 発行日 2012-10-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1078-8956 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11029600 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1038/nm.2928 | |||||
| 出版者 | ||||||
| 出版者 | Nature Publishing Group | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The class II α-isoform of phosphatidylinositol 3-kinase (PI3K-C2α) is localized in endosomes, the trans-Golgi network and clathrin-coated vesicles; however, its functional role is not well understood. Global or endothelial-cell-specific deficiency of PI3K-C2α resulted in embryonic lethality caused by defects in sprouting angiogenesis and vascular maturation. PI3K-C2α knockdown in endothelial cells resulted in a decrease in the number of PI3-phosphate-enriched endosomes, impaired endosomal trafficking, defective delivery of VE-cadherin to endothelial cell junctions and defective junction assembly. PI3K-C2α knockdown also impaired endothelial cell signaling, including vascular endothelial growth factor receptor internalization and endosomal RhoA activation. Together, the effects of PI3K-C2α knockdown led to defective endothelial cell migration, proliferation, tube formation and barrier integrity. Endothelial PI3K-C2α deficiency in vivo suppressed postischemic and tumor angiogenesis and diminished vascular barrier function with a greatly augmented susceptibility to anaphylaxis and a higher incidence of dissecting aortic aneurysm formation in response to angiotensin II infusion. Thus, PI3K-C2α has a crucial role in vascular formation and barrier integrity and represents a new therapeutic target for vascular disease. | |||||
| 内容記述 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | In Press / 2013-03-18公開予定. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
