Interaction of cortactin and Arp2/3 complex is required for sphingosine-1-phosphate-induced endothelial cell remodeling
Interaction of cortactin and Arp2/3 complex is required for sphingosine-1-phosphate-induced endothelial cell remodeling
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DOI：
10.1016/j.yexcr.2004.03.023
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发表时间：
2004-08-01
影响因子：
3.7
通讯作者：
Zhan, X
中科院分区：
文献类型：
--
作者：
Li, YS;Uruno, T;Zhan, X
1-磷酸鞘氨醇（SIP）诱导内皮细胞在Matrigel上形成毛细血管，伴随肌动蛋白组装和Corp 2/3复合物在细胞前缘的聚集。用corneumen反义寡核苷酸抑制corneumen表达显著损害SIP诱导的毛细血管形成、内皮细胞迁移和细胞周边肌动蛋白组装。过表达的野生型corneum标记的绿色荧光蛋白（GFP）增加SIP诱导的管形成和细胞运动，而过表达的突变体的细胞形成不良的毛细血管网络，并成为响应SIP的运动性降低。Triton X-100不溶性组分中的分布分析表明，corneum突变体抑制了野生型corneum和Arp 2/3复合物与肌动蛋白富集复合物的结合。此外，SIP介导的肌动蛋白聚合和Arp 2/3复合物的分布以及内源性coronin进入细胞前缘受到干扰。这些数据表明，corneum和Arp 2/3复合物之间的相互作用在SIP介导的内皮细胞重塑中起着重要作用。(C)2004年爱思唯尔公司All rights reserved.
Sphingosine-1-phosphate (SIP) induces capillary formation of endothelial cells on Matrigel in accompany with actin assembly and accumulation of cortactin and Arp2/3 complex at the cell-leading edge. Suppression of cortactin expression with a cortactin antisense oligo significantly impaired SIP-induced capillary formation, migration of endothelial cells, and actin assembly at the cell periphery. Overexpression of wild-type cortactin tagged by green fluorescent protein (GFP) increased the SIP-induced tube formation and cell motility, whereas the cells overexpressing the mutant formed poorly capillary network and became less motile in response to SIP. Analysis of distribution in Triton X-100 insoluble fractions demonstrated that the cortactin mutant inhibited the association of wild-type cortactin and Arp2/3 complex with the actin-enriched complex. Furthermore, actin polymerization at and distribution of Arp2/3 complex as well as endogenous cortactin into the cell-leading edge mediated by SIP was disturbed. These data suggest that the interaction between cortactin and Arp2/3 complex plays an important role in SIP-mediated remodeling of endothelial cells. (C) 2004 Elsevier Inc. All rights reserved.