Rosuvastatin inhibits homocysteine-induced smooth muscle cell phenotype transformation and its signal pathway / 西安交通大学学报(医学版)

ABSTRACT

ABSTRACTObjective To verify whether rosuvastatin can inhibit homocysteine (Hcy)‐induced rat aortic vascular smooth muscle cell (VSMC ) phenotype transformation and its potential mechanism .Methods The primary culture and identification of rat VSMCs were conducted , using VSMCs in passage4‐7 for the following experiments .The VSMCs were divided into 4 groupscontrol group ,Hcy (100μmol/L) group ,Hcy+ rosuvastatin group ,and Hcy+ rapamycin group .MTT was used to investigate the proliferation of VSMCs .Transwell chambers and wound healing were employed to test the migration ability of VSMCs . ICC was used to detect the VSMCs'morphology .Western blotting was used to investigate the expressions of SM‐actin ,SM‐MHC ,calponin ,OPN ,and p‐P70S6K1 in VSMCs of each group .Results Compared with those in control group , the proliferation and migration ability of VSMCs were significantly increased in Hcy modulation group (P< 0 .01) .The expressions of SM‐MCH and calponin increased but those of OPN and p‐P70S6K1 decreased in Hcy group compared with control group (P<0 .01) .The expression of SM‐actin did not significantly differ between the groups .Compared with those in Hcy modulation group , the proliferation and migration ability of VSMCs were significantly decreased in rosuvastatin and rapamycin groups ( P<0 .01) .The expressions of SM‐MCH and calponin increased while OPN and p‐P70S6K1 expressions decreased in rosuvastatin and rapamycin groups compared with Hcy group ( P< 0 .01 ) . Conclusion Hcy can induce the dedifferentiation of VSMCs ,and rosuvastatin can inhibit this effect of Hcy .Its potential mechanism may be realized via the mTOR/P70S6K1 signal pathway .