期刊
BLOOD
卷 109, 期 9, 页码 3745-3748出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-08-039925
关键词
-
类别
资金
- NCI NIH HHS [R01 CA039481, R01 CA 47282, R01 CA047282, R01 CA 39481] Funding Source: Medline
Endorepellin, a C-terminal fragment of the vascular basement membrane proteoglycan perlecan, inhibits angiogenesis via the alpha 2 beta 1-integrin receptor. Because this integrin is also implicated in platelet-collagen responses and because endorepellin or its fragments are generated in response to injury and inflammation, we hypothesized that endorepellin could also affect platelet biology. We discovered that endorepellin supported alpha 2 beta 1-dependent platelet adhesion, without appreciably activating or aggregating platelets. Notably, endorepellin enhanced collagen-evoked responses in platelets, in a src kinase-dependent fashion, and enhanced the collagen-inhibitory effect of an alpha 2 beta 1-integrin function-blocking antibody. Collectively, these results suggest that endorepellin/alpha 2 beta 1-integrin interaction and effects are specific and dependent on cell type, differ from those emanated by exposure to collagen, and may be due to cellular differences in alpha 2 beta 1-integrin activation/ligand affinity state. These studies also suggest a heretofore unrecognized role for angiostatic basement membrane fragments in platelet biology. (C) 2007 by The American Society of Hematology.
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