LncRNA HOTAIR regulates the proliferation and apoptosis of vascular smooth muscle cells through targeting miRNA-130b-3p/PPARα axis

OBJECTIVE: To investigate the role of long non-coding RNA (lncRNA) HOTAIR in influencing the proliferative and apoptotic abilities of vascular smooth muscle cells (VSMCs) by regulating microRNA-130b-3p (miRNA-130b-3p)/peroxisome proliferator-activated receptor alpha (PPAR alpha) axis. MATERIALS AND METHODS: The expression levels of HOTAIR, miRNA-130b-3p, and PPAR alpha in VSMCs treated with different doses of oxLDL for different time points were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The subcellular distribution of HOTAIR in VSMCs was examined. The regulatory effects of HOTAIR, miRNA-130b-3p. and PPAR alpha on the viability and apoptosis of oxLDL-treated with VSMCs were assessed. The interaction among HOTAIR, miRNA-130b-3p, and PPAR alpha was evaluated through Dual-luciferase reporter gene assay and Western blot. RESULTS: After treatment of different doses of ox-LDL in VSMCs, the levels of HOTAIR and PPAR alpha were gradually downregulated, whereas miRNA-130b-3p was upregulated. The over-expression of HOTAIR reversed the enhanced viability and suppressed apoptosis in ox-LDL-treated VSMCs. HOTAIR was mainly distributed in nucleus of VSMCs. MiRNA-130b-3p was the direct target of HOTAIR and its level was negatively regulated by HOTAIR. Moreover, miRNA-130b-3p could bind to PPAR alpha and could negatively regulate its level. The knockdown of HOTAIR could reverse the regulatory effect of PPAR alpha on the proliferative and apoptotic abilities of VSMCs CONCLUSIONS: HOTAIR reduces the proliferative ability and stimulates the apoptosis in ox-LDL-treated VSMCs by targeting miRNA-130b-3p/PPAR alpha axis.