The Effects Of Rho-Associated Kinase In VEGF Mediated Angiogenesis, Cell Proliferation And Migration

Objection:This study was designed to investigate under hypoxia-mimicking conditions, the effects of ROCKs in VEGF paracrine and autocrine loop formation, cell morphology, migration and proliferationMethods and Results:cell groups:normal group and control group (C), hypoxia+the control silence group (NC), hypoxia+ROCK1silence group (R1), hypoxia+ROCK2silence group (R2), hypoxia+ROCKl+ROCK2silence group (R1+R2), hypoxia+fasudil group (group F). Transfection groups were used100nmol/L siRNA to transfect for6h, then continue to cultivate in complete medium for12h. F group was treated with50nmol/L fasudil for2h. Then, all treated cells were induced with200μmol/L cocl2to mimic hypoxic environment for6h. Results:Treatment with ROCK2siRNA, ROCKs siRNA or fasudil can prevent HIF-1α-driven, VEGF-mediated paracrine and autocrine loop formation. The number of cell migration significantly increased and cell proliferation rate accelerat ed in hypoxia. Treatment with ROCK2siRNA, ROCKs siRNA or fasudil was completely prevented MBS phosphorylation, reducing the migration. But R1group was not significantly inhibited the expression of P-MBS. There was no difference in the ability of regulating he cell proliferation rate between ROCKland ROCK2.Conclusion:ROCKs is an essential mechanism for HIF-1α-driven, VEGF-mediated paracrine and autocrine loop formation, and participate in maintaining cell shape, regulating cell proliferation and migration. Howere, There was some difference in the ability of inhibiting the expression of P-MBS between ROCKland ROCK2.