DOWN-REGULATION OF MIR-3568 PROMOTES PROLIFERATION AND MIGRATION OF VASCULAR SMOOTH MUSCLE A7R5 CELLS BY REGULATING AKT/FOXO1 SIGNALLING PATHWAY

Yan Lu¹, Nan Gao², Pengkang Yang¹, Shaojuan Yu¹, Yuqiang Ji¹, Chao Zhao¹, Yuan Lu^{1, *} 

¹Department of Cardiovascular Medicine, Xi’an First Hospital, Xi’an 710002, PR China - ²Xi’an Fourth Hospital, Xi’an 710004, PR China

Objective: To investigate the effect of down-regulation of micro-ribonucleic acid 3568 (miRNA-3568) on the proliferation and migration of vascular smooth muscle A7r5 cells by regulating the protein kinase B (Akt) and forkhead framework transcription protein (Fox) signalling pathway. 

Methods: The rat thoracic aorta smooth muscle cell line A7r5 was selected and randomly divided into an anti-miR-ctrl group and anti-miR-3568 group. The anti-miR-ctrl group was transfected with a 20nM miR-3568 inhibitor, and the anti-miR-3568 group was transfected with the same amount of control RNA. The proliferation rate and migration distance of A7r5 cells in the two groups were compared, and the expression levels of miR-3568, FoxO1, p-FOXO1, Akt and p-AKT in A7r5 cells in the two groups were compared. 

Results: Compared with the anti-miR-ctrl group, the expression level of miR-3568 protein in A7r5 cells of the anti-miR-3568 group was significantly reduced (P<0.05). Compared with the anti-miR-ctrl group, the proliferation rate of A7r5 cells in the anti-miR-3568 group was significantly increased (P<0.05). The migration distance of A7r5 cells in the anti-miR-3568 group was significantly increased (P<0.05) compared with the anti-miR-ctrl group. Compared with the anti-miR-ctrl group, the expression levels of p-FOXO1, p-AKT (S473) and p-AKT (T308) in A7r5 cells in the anti-miR-3568 group were significantly increased, and the expression levels of FoxO1 were significantly decreased (P<0.05). 

Conclusion: Down-regulation of the expression level of miR-3568 can significantly promote the proliferation and migration of vascular smooth muscle A7r5 cells, possibly through the regulation of the Akt/FoxO1 signalling pathway.