miR-155-5p inhibits the viability of vascular smooth muscle cell via targeting FOS and ZIC3 to promote aneurysm formation.

As the most common form of aortic aneurysm, abdominal aortic aneurysm (AAA) is associated with the proliferation and apoptosis of vascular smooth muscle cells (VSMCs). Our present study found that during HO or NaAsO induced injury of VSMC, the expression of miR-155-5p significantly increased. While silencing of miR-155-5p can attenuate HO or NaAsO suppressed viability and induced apoptosis of VSMCs. In silico analysis and western blot analysis suggested that miR-155-5p can suppress the expression of FOS and ZIC3 in VSMCs by targeting their 3'UTR. Over expression of FOS or ZIC3 can abolish HO treatment and miR-155-5p induced suppression of VSMC viability. The inhibitor of NF-κB (p65), while not STAT3, can abolish HO induced expression of miR-155-5p and cell apoptosis. In addition, HO treatment can increase the phosphorylation and nuclear translocation of p65 in VSMCs. The expression of miR-155-5p in cells isolated from participants diagnosed with AAA were significantly greater than that in the normal group. Further, miR-155-5p was negative correlated with the expression of FOS and ZIC3 in cells from AAA patients. Collectively, miR-155-5p can regulate the viability and apoptosis of VSMCs to trigger the progression of AAA. It might be an effective therapeutic target for the treatment of AAA in clinical practice.