Cheng Chun, Liu Haiou, Ge Haiyan, Qian Ji, Qin Jing, Sun Linlin, Shen Aiguo
Institute of Nautical Medicine, Nantong University, Nantong 226001, China.
Biochem Biophys Res Commun. 2007 Jun 22;358(1):342-8. doi: 10.1016/j.bbrc.2007.04.147. Epub 2007 Apr 30.
Integrin-mediated substrate adhesion of endothelial cells leads to dynamic rearrangement of the actin cytoskeleton. Protein kinase C (PKC) stimulates reorganization of microfilaments and adhesion, but the mechanism by which this occurs is unknown. Src suppressed C kinase substrate (SSeCKS) is a PKC substrate that may play an important role in regulating actin cytoskeleton. We found that SSeCKS was localized to focal adhesion sites soon after cell adhesion and that SSeCKS translocated from the membrane to the cytosol during the process of cell spreading. Using small interfering RNAs specific to SSeCKS, we show that RPMVEC cells in which SSeCKS expression was inhibited reduce adhesion and spread on LN through blocking the formation of actin stress fibers and focal adhesions. These results demonstrated SSeCKS modulate endothelial cells adhesion and spreading by reorganization of the actin cytoskeleton.
整合素介导的内皮细胞与底物的黏附导致肌动蛋白细胞骨架的动态重排。蛋白激酶C(PKC)刺激微丝重组和黏附,但发生这种情况的机制尚不清楚。Src抑制性C激酶底物(SSeCKS)是一种PKC底物,可能在调节肌动蛋白细胞骨架中起重要作用。我们发现,细胞黏附后不久,SSeCKS就定位于黏着斑部位,并且在细胞铺展过程中,SSeCKS从膜转移到细胞质中。使用针对SSeCKS的小干扰RNA,我们表明,SSeCKS表达受到抑制的RPMVEC细胞通过阻断肌动蛋白应力纤维和黏着斑的形成,减少了在层粘连蛋白上的黏附与铺展。这些结果表明,SSeCKS通过肌动蛋白细胞骨架的重组来调节内皮细胞的黏附与铺展。