The effect of RhoA on human umbilical vein endothelial cell migration and angiogenesis in vitro

被引：2

作者：

Zhao, LP ^{[1
]}

Xu, G ^{[1
]}

Zhou, JF ^{[1
]}

Xing, H ^{[1
]}

Wang, SX ^{[1
]}

Wu, MF ^{[1
]}

Lu, YP ^{[1
]}

Ma, D ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Canc Biol Res Ctr, Wuhan 430030, Hubei, Peoples R China

来源：

ONCOLOGY REPORTS | 2006年 / 15卷 / 05期

关键词：

RhoA; human umbilical vein endothelial cells; migration; angiogenesis;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The mechanisms that control the morphologic organization of endothelial cells (ECs) into new blood vessels are not well understood. Recent studies revealed that the small G proteins of the Rho family are key regulators of cell migration, involving reorganization of the actin cytoskeleton, cell migration and the regulation of gene transcription. We hypothesized that RhoA GTPase, a member of the Rho family, may play an important role in EC organization during angiogenesis, the process of new vessel formation in pre-existing tissues. To test this hypothesis, we investigated the effects of RhoA on human umbilical vein endothelial (HUVE) cell migration and angiogenesis in vitro, by stably transfecting HUVE cells with sense RhoA expression plasmid through the Lipofect-2000 system. Wound assay in vitro and 3-dimensional cell culture were used to detect the migration and angiogenesis capacity of HUVE cells. The morphological changes of transfected cells were revealed under confocal and phase contrast microscopy. Our results demonstrated that the increased expression of RhoA in HUVE cells significantly enhanced the morphogenetic changes and cytoskeletal reorganization of the transfected cells, and also enhanced cell migration and angiogenic capacity in vitro, suggesting that RhoA plays an important role in the process of HUVE cell migration and angiogenesis in vitro.

引用

页码：1147 / 1152

页数：6

共 27 条

[1] RhoA induces MMP-9 expression at CD44 lamellipodial focal complexes and promotes HMEC-1 cell invasion [J].