Abstract
This study investigated the regulatory role of long non-coding RNA (lncRNA) MALAT1 in HA-VSMCs proliferation and apoptosis through mediating PTEN level. HA-VSMCs were induced with different doses of ox-LDL for various time points, and the relative level of MALAT1 was determined. MALAT1 was upregulated in a time- and dose-dependent manner. Overexpression of MALAT1 increased viability and proliferative rate, and decreased apoptotic rate of HA-VSMCs induced with 100 mg/L ox-LDL for 24 h, which was reversed by si-MALAT1 transfection. PTEN protein level was downregulated by ox-LDL induction and upregulated by si-MALAT1. MALAT1 was mainly distributed in the nucleus, and it interacted with EZH2. Silencing of MALAT1 attenuated EZH2 binding on PTEN promoter region. Knockdown of PTEN reversed the decreased proliferative ability and increased apoptotic rate in ox-LDL-induced HA-VSMCs transfected with si-MALAT1. These results indicate that MALAT1 accelerates HA-VSMCs proliferation by recruiting EZH2 to mediate PTEN level. Overall, MALAT1 may play a crucial role in the progression of atherosclerosis and may be a potential therapeutic target.
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