MiR-27b-3p Correlates with Arteriosclerosis Obliterans and Promotes the Proliferation and Migration of Arterial Smooth Muscle Cells by Targeting GAB1.

Patients with atherosclerosis obliterans (ASO) are at risk of amputation or even death if timely treatment is not provided; current clinical treatments for ASO have certain disadvantages. This study aimed to ascertain the function of miR-27b-3p in ASO to provide novel insights for ASO treatment.The expression of miR-27b-3p in the serum of 117 ASO subjects and 80 healthy individuals was assessed by polymerase chain reaction. Risk factors for coronary artery disease (CAD) in ASO were assessed by multivariate logistic regression analysis. The atherosclerosis cell model was conducted using human vascular smooth muscle cells (HVSMCs) induced with oxidized low-density lipoprotein (ox-LDL). The interaction relationship between miR-27b-3p and GAB1 was assessed using a dual-luciferase reporter assay. HVSMC proliferation and migration were analyzed using the cell counting kit-8 and transwell assay.MiR-27b-3p was upregulated in ASO; it was correlated with ASO severity indicators (ankle-brachial index level and Fontaine stage) and identified as a risk factor for CAD incidence in ASO. Ox-LDL induction in HVSMCs promoted HVSMC proliferation and migration. Overexpression of miR-27b-3p facilitated the proliferation and migration of ox-LDL-induced HVSMCs, which were attenuated by GAB1 overexpression.The upregulation of miR-27b-3p in ASO was correlated with ASO severity and served as a risk factor for CAD in patients with ASO. The potential regulatory mechanism of miR-27b-3p in ASO was the acceleration of vascular smooth muscle cell proliferation and migration by targeting GAB1.