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首页> 外文期刊>Journal of Cellular Physiology >Endothelial cell apoptosis in capillary network remodeling.
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Endothelial cell apoptosis in capillary network remodeling.

机译：内皮细胞凋亡在毛细管网重构。

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摘要

We hypothesized that the regulation of apoptosis is an important determinant of capillary network structure. Using human umbilical vein endothelial cells (HUVEC) in in vitro model systems of capillary tube formation, we initially documented that apoptosis is a prominent feature of network formation. Perturbations of integrin-matrix signaling by the administration of either colchicine or an anti-alpha(v)beta3 antibody resulted in the dissolution of the tubular network in association with increased apoptosis. The activation of the alpha(v)beta3 integrin induced increased expression of the anti-apoptotic gene bcl-2 and conferred resistance to the proapoptotic effect of TGF-beta1. In contrast to the stable networks formed by HUVEC, bovine aortic endothelial cells (BAEC) exhibited a more dynamic process of network formation and spontaneous involution. The inhibition of BAEC apoptosis by stable transfection of bcl-2 prevented the involution of the network. We hypothesized that TGF-beta1 present within the model system mediated network involution by inducing BAEC death. Indeed, blockade of TGF-beta1 with neutralizing antibodies reduced BAEC apoptosis and preserved the network structure. As observed with HUVEC networks, stable BAEC networks formed during blockade of TGF-beta1 were also dependent on the survival-promoting effects of matrixintegrin interactions. This study suggests that capillary network structure is determined by the balance of proapoptotic vs. anti-apoptotic signals mediated by the engagement of cytokine and integrin receptors within the milieu.
机译：我们假设细胞凋亡的调节是一个重要的行列式毛细管网吗结构。细胞(HUVEC)在体外模型系统毛细管的形成,我们最初记录细胞凋亡是一个网络的显著特征形成。信号的管理秋水仙碱或anti-alpha (v) beta3抗体导致了管状的解体网络与细胞凋亡增加。α(v)的激活beta3整合素诱导的表达增加抗凋亡基因bcl - 2和授予抵抗的proapoptotic效应TGF-beta1。由HUVEC,牛主动脉内皮细胞(BAEC)表现出一个更动态的过程网络形成和自发的退化。抑制BAEC凋亡的稳定转染的bcl - 2防止退化网络。现在在系统介导的网络模型对合诱导BAEC死亡。封锁TGF-beta1中和抗体减少BAEC凋亡和保存网络结构。网络,稳定BAEC网络中形成封锁TGF-beta1也依赖于survival-promoting matrixintegrin的影响交互。网络结构是由之间的平衡决定的proapoptotic与抗凋亡信号调节细胞因子的参与,整合素环境内的受体。

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