期刊
DEVELOPMENT
卷 141, 期 7, 页码 1465-1472出版社
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.104539
关键词
Angiogenesis; Endocytosis; Endothelium; Mouse
资金
- National Institutes of Health [HL64793, HL61371, HL081190, HL096670, PO1 1070205, RO1 GM068600, GM088240]
- Grants-in-Aid for Scientific Research [24658243] Funding Source: KAKEN
Here we show that dynamin 2 (Dnm2) is essential for angiogenesis in vitro and in vivo. In cultured endothelial cells lacking Dnm2, vascular endothelial growth factor (VEGF) signaling and receptor levels are augmented whereas cell migration and morphogenesis are impaired. Mechanistically, the loss of Dnm2 increases focal adhesion size and the surface levels of multiple integrins and reduces the activation state of beta 1 integrin. In vivo, the constitutive or inducible loss of Dnm2 in endothelium impairs branching morphogenesis and promotes the accumulation of beta 1 integrin at sites of failed angiogenic sprouting. Collectively, our data show that Dnm2 uncouples VEGF signaling from function and coordinates the endocytic turnover of integrins in a manner that is crucially important for angiogenesis in vitro and in vivo.
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