Mechanical-chemical interaction and its mechanobiological mechanism on the migration of endothelial cells

Objective To elucidate the mechanical chemical interaction and its mechanobiological mechanism on the migration of endothelial cells. Method RT-PCR, Western blot and immunofluorescence were applied to detect the expression of CXCR1 and CXCR2 and their distributions under three levels of shear stress; anti-IL8RA and anti-IL8RB were used to inhibit CXCR1 and CXCR2 to evaluate endothelial cell migration under shear stress; ECs were transfected to obtain the wild type Rac1(Rac1WT) or RhoA (RhoAWT), the constitutively active forms of Rac1(Rac1Q61L) or RhoA (RhoA63L), and the dominant negative forms of Rac1(Rac1T17N) or RhoA (RhoA188A) respectively, with lipofectamine 2000 reagent. ECs transfected with three plasmids of Rac1 were exposed to three levels of shear stress and IL-8, respectively; ECs transfected with three plasmids of RhoA were stimulated by IL-8. Results CXCR1 and CXCR2 are novel mechano sensors mediating laminar shear stress induced endothelial cell migration. High expression of Rac1 and RhoA can promote EC migration, while their low expression inhibits EC migration. Conclusions CXCR1, CXCR2, Rac1 and RhoA are critical signaling molecules in mechanical chemical interaction of EC migration.