Dysfunctions of vascular endothelial permeability are related to a number of human diseases such as atherosclerosis, high blood pressure, stroke, inflammation, cancer, diabetes-induced retinopathy, macular edema and so on. Shear stress is an important mechanical force that affects vascular endothelial cells. It plays a particular role in permeability regulation. Rho GTPases is a family of small G proteins which act as cell signal molecules. They are assumed to mediate the regulation of the permeability of vascular endothelial cells. In this paper review is given on how shear stress regulates the permeability of vascular endothehal cells as well as the in-fluence of Rho GTPases on the role in molecular mechanism. It is suggested that shear stress-regulated vascular endothelial permeability is mediated by Rho GTPases.

This study was conducted to elucidate the effects of different fluid shear stress on the expression of IL-8 receptors CXCR1 in endothelial cells. The HUVEC cell lines, EA. Hy926 cells, were cultured in vitro, exposed to 5.56, 10.02, and 15.27 dyn/cm2 laminar shear stress, respectively, and then the shear stress grous were each investigated at the time-points of 0h, 1h, 2h, 4h and 8h. Western blotting was used for detecting the expression of IL-8 receptor CXCR1 at the time-points. The results showed that, under 5.56 dyn/cm2 shear stress, the expression of CXCR1 increased with time significantly (P < 0.01). The maximum expression of CXCR1 appeared at 4 h and was 2.2 times that of the control. When exposed to 10.02 dyn/cm2, the expression of CXCR1 increased gradually with time and finally remained at a constant higher level. When exposed to 15.27 dyn/cm2, CXCR1 expression decreased significantly with time (P < 0.01). The minimum CXCR1 expression appeared at 8 h and was 62. 59 percent of that of the control. These results indicate that the expression of CXCR1 in endothelial cell is regulated by laminar shear stress.
Cell Line ; Endothelial Cells ; cytology ; metabolism ; Humans ; RNA, Messenger ; biosynthesis ; genetics ; Receptors, Interleukin-8A ; genetics ; metabolism ; Shear Strength ; Stress, Mechanical ; Umbilical Veins ; cytology