LINC00473 inhibits vascular smooth muscle cell viability to promote aneurysm formation via miR-212-5p/BASP1 axis.

Abdominal aortic aneurysm (AAA), as the most common type of aortic aneurysm, is closely related to the proliferation and apoptosis ability of vascular smooth muscle cells (VSMCs). Long non-coding RNAs (lncRNAs) are emerging regulators in disease development. LncRNA LINC00473 has been shown to affect cell proliferation and apoptosis in various cancers, but its role in AAA is still blank. In this work, in vitro AAA models were successfully established since cell viability was inhibited whereas apoptosis stimulated in VSMCs treated with H2O2. LINC00473 was up-regulated in VSMCs after H2O2 treatment. Overexpression of LINC00473 inhibited VSMC cell proliferation and promoted cell apoptosis and its silence mitigated H2O2-induced injuries to VSMCs. Additionally, we uncovered that LINC00473 sponged miR-212-5p to regulate brain acid soluble protein 1 (BASP1) expression. Finally, rescue assays uncovered that overexpression of miR-212-5p or suppression of BASP1 reversed the effects of LINC00473 up-regulation on cell proliferation and cell apoptosis. And the positive correlation between LINC00473 and BASP1 as well as the negative relation of miR-212-5p to both LINC00473 and BASP1 were confirmed in AAA tissues. All finding illuminated that LINC00473 participated in AAA development by regulating miR-212-5p/BASP1 pathway, suggesting LINC00473 as a promising target for AAA therapy.