microRNA-762 regulate vascular smooth muscle cell phenotypic switch through targeting STAT3 in aortic dissection

Background this study aimed to evaluate the effect of microRNA-762/stat3 axis on VSMCs phenotypic switch in aortic dissection (AD). Method targetscan and miRDB bio-informatics analysis were used to verify the potential binding sites between microRNA-762 and stat3. qRT-PCR and western blot confirmed different expression of microRNA-762, stat3 and phenotypic switch markers such as SM22α, calponin, SMA and MYH11 between aortic dissection and normal aortic tissues. CCK8 assay and PCNA were used to present the proliferative capacity. Transwell migration assay, MMP2 and MMP9 were used to show the migration ability. Dual luciferase reporter assay was used to demonstrate the binding sites between microRNA-762 and stat3. Results microRNA-762 was downregulated in human AD tissues. Meantime, phenotypic switch markers showed low expression in AD tissues. Over expression of microRNA-762 through RNA interference weakened VSMC proliferation and migration and promoted the expression of phenotypic switch markers. Bio-informatics analysis presented that microRNA-762 had binding sites with stat3, which confirmed by dual luciferase reporter assay in HEK293T. Co-transfect with microRNA-762 mimic and stat3 vector could rescue the proliferation and migration ability causing by transfect with microRNA-762 mimic only. Conclusions low expression of microRNA-762 promote phenotypic switch by targeting stat3 in VSMCs, which could be used as a potential diagnostic marker and therapeutic target for AD.