期刊
CIRCULATION RESEARCH
卷 92, 期 3, 页码 300-307出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.RES.0000055016.36679.23
关键词
focal adhesion kinase; vasculogenesis; angiogenesis; fibronectin; endothelial cell differentiation
资金
- NCI NIH HHS [KO1 CA87652] Funding Source: Medline
- NHLBI NIH HHS [HL 35753] Funding Source: Medline
The nonreceptor tyrosine kinase focal adhesion kinase (FAK) is a point of convergence for signals from extracellular matrix, soluble factors, and mechanical stimuli. Targeted disruption of the fak gene in mice leads to death at embryonic day 8.5 (E8.5). FAK(-/-) embryos have severely impaired blood vessel development. Gene expression and in vitro differentiation studies revealed that endothelial cell differentiation was comparable in FAK(-/-) and wild-type E8.5 embryos. We examined the role of FAK in blood vessel morphogenesis using an in vitro tubulogenesis assay and three different culture systems: FAK(+/+) and FAK(-/-) embryoid bodies, FAK(+/+) and FAK(-/-) endothelial cells, and human umbilical vein endothelial cells expressing antisense FAK, a dominant- negative fragment of FAK, or wild-type FAK. In all of these systems, endothelial cells deficient in FAK expression or function displayed a severely reduced ability to form tubules in Matrigel. These studies demonstrate clearly that the vascular defects in FAK(-/-) mice result from the inability of FAK-deficient endothelial cells to organize themselves into vascular networks, rather than from defects in tissue-specific differentiation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据