miR-378c suppresses VSMCs phenotypic modulation. (A) qRT-PCR analysis of SM α-actin, calponin and miR-378c in VSMCs stimulated with PDGF-BB for 48 h after 24 h serum withdrawal. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with non-PDGF treated group. (B) qRT-PCR analysis of SM α-actin, calponin and miR-378c in serum-starved (0.1%) VSMCs. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with 0 h group. (C) qRT-PCR analysis of SM α-actin, calponin and miR-378c in VSMCs treated with PDGF-BB after 24 h serum withdrawal. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with 0 h group. (D) VSMCs stimulated with PDGF-BB for 48 h were further transfected with miR-378c mimic or mimic control, SM α-actin and calponin were analyzed by qRT–PCR. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with non-PDGF-treated group; #P < 0.05 as compared with PDGF-treated mimic control group. (E) VSMCs stimulated with PDGF-BB were further transfected with miR-378c inhibitor or vehicle (DMSO), VSMC differentiation markers SM α-actin and calponin were analyzed by qRT–PCR. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with non-PDGF-treated group; #P < 0.05 as compared with PDGF-treated vehicle group. (F) VSMCs stimulated with PDGF-BB were further transfected with miR-378c mimic or mimic control, cell numbers were examined. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with PDGF-treated mimic control group. (G) VSMCs stimulated with PDGF-BB were further transfected with miR-378c inhibitor or vehicle (DMSO), cell numbers were examined. Data were presented as mean ± SD, n = 4. *P < 0.05 as compared with PDGF-treated vehicle group.