SNHG8/miR-873-3p/CDK6 axis triggers proliferation and migration of smooth muscle cells in intimal hyperplasia

Long-strand non-coding RNAs play a crucial role in intimal hyperplasia. Nevertheless, the mechanism by which small nucleolar RNA host gene 8 affects intimal hyperplasia remains unknown.

The expression levels of SNHG8, miR-873-3p, and CDK6 were detected by qRT-PCR or Western blotting. Cell proliferation was measured using 5-ethynyl-2'-deoxyuridine and cell counting kit-8 assay. Cell migration was detected by Transwell and scratch assay. The binding roles and sites of miR-873-3p to SNHG8 and CDK6 were detected by dual luciferase reporter gene assay. The binding role of miR-873-3p and SNHG8 was detected by RNA immunoprecipitation assay. Vascular injury was simulated by ligation of the left common carotid artery.

This study suggests that the high expression of SNHG8 in intimal hyperplasia vascular smooth muscle cells can function as a competitive endogenous RNA. By specifically binding to miR-873-3p, which is weakened, SNHG8 acts as a negative regulator of CDK6 target genes, leading to upregulation of CDK6 expression. This interaction was also shown to promote vascular smooth muscle cells proliferation and migration.

This study revealed a novel regulatory mechanism of action of the SNHG8/miR-873-3p/CDK6 axis in the progression of intimal hyperplasia and points to the potential of SNHG8, miR-873-3p, and CDK6 as novel targets for the diagnosis and treatment of intimal hyperplasia.