OUYANG Yong,LIU Yan,YE Yangbo. Effect of miR-19a on proliferation and migration of vascular smooth muscle cells and inflammatory infiltration in abdominal aortic aneurysm[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2020, 50(8): 609-615，622.
Abstract：Objective: To investigate the effect of miR-19a on proliferation and migration of vascular smooth muscle cells and inflammatory infiltration through targeting CDKN2B in abdominal aortic aneurysm (AAA) and its underlying mechanism. Methods: Serum samples were collected from 15 patients without any treatment after primary AAA, 15 healthy persons during the same period, and samples of AAA tissues and without AAA tissues were collected from 15 patients. RT-qPCR was used to detect the expression of miR-19a. CCK-8, Transwell, and flow cytometry were respectively performed to examine the proliferation, migration and apoptosis of vascular smooth muscle cells. Inflammatory cytokines secretion of THP-1 cells were evaluated using
enzyme-linked immunosorbent assay (ELISA). The expression of protein was measured by western blot. Dual-luciferase reporter gene assay was applied to verify the interaction relationship between miR-19a and CDKN2B. Results: Compared with the control group, miR-19a was significantly overexpressed in the serum samples and tissues of AAA patients. Knockdown of miR-19a markedly suppressed cell proliferation, migration and induced apoptosis of vascular smooth muscle cells. Silencing of miR-19a significantly decreased the levels of inflammatory cytokines and matrix metalloproteinase. Dual-luciferase reporter gene assay results showed that miR-19a decreased the expression of CDKN2B by binding to its 3’-untranslated region (UTR). Upregulation of CDKN2B attenuated the inhibitory effect of miR-19a-elevated on the proliferation and migration of vascular smooth muscle cells and inflammatory response of THP-1 cells. Conclusion: Knockdown of miR-19a could alleviate the development of AAA by inhibiting the proliferation and migration of smooth muscle cells and down regulating inflammatory cell infiltration, which its mechanism is to target up-regulation of CDKN2B expression.
