LncRNA UCA1 sponges miR-26a to regulate the migration and proliferation of vascular smooth muscle cells.

BACKGROUND: Recent studies have shown that the long non-coding RNA urothelial carcinoma-associated (UCA1) plays a key role in cardiovascular injury. However, the potential biological role of UCA1 in progression of atherosclerosis (AS) remains unclear. The aim of the present study is to identify the regulation of lncRNA UCA1 on atherosclerosis-related vascular dysfunction via miR-26a targeting phosphatase and tensin homolog (PTEN), and investigate the underlying mechanisms in the development of atherosclerosis.

METHODS: The proliferation and migration were detected using CCK-8 assay, Wound healing assay and Transwell assay. The expression of miR-26a and its target gene in vascular smooth muscle cells was detected by qRT-PCR, the complementary binging of miRNA and lncRNA was verified by luciferase assays. PTEN was predicted to be the target of miR-26a and the prediction was verified by luciferase assays.

RESULTS: Expression of miR-26a was up-regulated in ox-LDL (50 mg/l) induced vascular smooth muscle cell (VSMCs), and overexpression of miR-26a inhibited PTEN expression and promoted PCNA α-SMA and SM22-α expression (qRT-PCR and WB).

CONCLUSION: The expression of UCA1 antagonized the effect of miR-26a on the downregulation of its target PETN and contraction phenotype. This study reveals that lncRNA UCA1 act as an endogenous sponge of miR-26a and downregulates miR-26a expression levels, and thereby relieving the inhibition of its target gene PTEN and alleviates VSMCs proliferation against atherosclerosis.