The role of αv integrins during angiogenesis:: insights into potential mechanisms of action and clinical development
The role of αv integrins during angiogenesis:: insights into potential mechanisms of action and clinical development
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DOI：
10.1172/jci6869
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发表时间：
1999-05-01
影响因子：
15.9
通讯作者：
Cheresh, DA
中科院分区：
文献类型：
--
作者：
Eliceiri, BP;Cheresh, DA
本系列在本期的第1231-1236页和1237-1241页上继续。可以预测，αvβ3与αvβ3之间的物理结合不仅可能促进细胞外基质的重塑，而且可能使αvβ3介导的内皮细胞通过附着到暴露的RGD位点经蛋白分解的基质而侵袭。在最近的研究中，被称为PEX的基质金属蛋白酶-2的自然分解片段被证明在经历了新生血管的组织中积累(13)。事实上，重组PEX不仅能够阻断基质金属蛋白酶-2与αvβ3的结合，而且当在体内给药时，能够阻断肿瘤相关的血管生成(13)。因此，PEX不仅可以阻止基质金属蛋白酶-2介导的内皮细胞基质重塑，而且可以通过消除胶原中暴露的RGD位点来阻止α与β3的连接。
This series continues on pages 1231–1236 and 1237–1241 in this issue. exposed and become ligated to αvβ3. One might predict that the physical association between MMP-2 and αvβ3 might not only facilitate ECM remodeling but would enable αvβ3-mediated endothelial cell invasion through the proteolyzed matrix by attachment to exposed RGD sites. In recent studies, natural breakdown fragments of MMP-2, termed PEX, were shown to accumulate in tissues that had undergone neovascularization (13). In fact, recombinant PEX was not only able to block MMP-2 binding to αvβ3 but when administered in vivo was able to disrupt tumor-associated angiogenesis (13). Thus, PEX not only prevents endothelial cell–mediated matrix remodeling by MMP-2 but would preclude αvβ3 ligation by elimination of the exposed RGD sites in collagen.