Objective : To investigate the effect of miR-206-3p on the function of vascular smooth muscle cells and its possible involvement in the pathogenesis of aortic dissection,and to provide new clues for the pathogenesis of aortic dissection.Methods:Peripheral serum was collected from 50 patients with clinically diagnosed acute aortic dissection and 50 healthy controls.First,q PCR was used to detect the relative expression level of miR-206 in the serum of the two groups.CCK8 assay,cell scratch assay and Western blot were used to verify the effects of miR-206-3p on the proliferation,migration and phenotypic transformation of vascular smooth muscle cells.The downstream target genes of miR-206-3p were predicted by bioinformatics,and the targeting relationship between miR-206-3p and TMSB4 X was verified by Western blot and dual luciferase reporter assay.Finally,CCK8,cell scratch,Western blot and other experiments were used to verify the role of miR-206-3p in the pathogenesis of aortic dissection by targeting TMSB4 X to regulate the physiological function of vascular smooth muscle cells.Results:q PCR showed that miR-206 was highly expressed in the serum of patients with acute aortic dissection compared with the control group(p=0.0014).The results of CCK8,cell scratch assay and Western blot showed that miR-206-3p mimics could inhibit the proliferation,migration and phenotype transition of vascular smooth muscle cells compared with NC mimics,and the differences were statistically significant(P<0.05);Bioinformatics showed that TMSB4 X was the downstream target gene of miR-206-3p,and Western blot and dual luciferase reporter assay confirmed that miR-206-3p had a negative regulatory relationship with TMSB4 X.Finally,the results of CCK8 and Western blot showed that overexpression of TMSB4 X reversed the inhibitory effects of up-regulated miR-206-3p on the proliferation and phenotypic switching of vascular smooth muscle cells(P<0.05);However,there was no difference in cell migration assay among the groups.Conclusions:miRNA-206-3p participates in the pathogenesis of aortic dissection by targeting TMSB4 X to regulate the proliferation,migration,and phenotypic switching of vascular smooth muscle cells. |