长链非编码RNA UCA1通过调控miR-132/Lrrfip1轴促进血管平滑肌细胞增殖。
lncRNA UCA1 regulates miR-132/Lrrfip1 axis to promote vascular smooth muscle cell proliferation.
作者信息
Chen Wenming, Zhao Wei, Hao Minghui, Wang Yuping
机构信息
Department of Cardiology, Beijing Luhe Hospital, Capital Medical University, No. 82, Xinhua South Street, Tongzhou District, Beijing City, 101100, PR China.
Department of Cardiology, Beijing Luhe Hospital, Capital Medical University, Beijing City, 101100, PR China.
出版信息
Open Med (Wars). 2023 Jul 25;18(1):20230738. doi: 10.1515/med-2023-0738. eCollection 2023.
UCA1 is predicted to bind to miR-132, which is a key player in the proliferation of vascular smooth muscle cells (VSMCs). This research studied the role of lncRNA UCA1 in atherosclerosis. The binding of UCA1 to miR-132 was proved by dual luciferase activity assay and RNA immunoprecipitation. UCA1 and miR-132 failed to affect each other's expression in VSMCs. UCA1 was upregulated and miR-132 was decreased in atherosclerosis plasma. However, they are not closely correlated across atherosclerosis and control plasma sample. Interestingly, UCA1 suppressed the role of miR-132 in downregulating Lrrfip1 expression and promoting VSMC proliferation. Therefore, UCA1 is downregulated in atherosclerosis and may regulate miR-132/Lrrfip1 axis to promote VSMC proliferation.
UCA1被预测可与miR-132结合，而miR-132是血管平滑肌细胞（VSMC）增殖的关键因子。本研究探讨了长链非编码RNA UCA1在动脉粥样硬化中的作用。通过双荧光素酶活性测定和RNA免疫沉淀证实了UCA1与miR-132的结合。UCA1和miR-132在VSMC中未能相互影响对方的表达。在动脉粥样硬化血浆中，UCA1上调而miR-132降低。然而，在动脉粥样硬化血浆样本和对照血浆样本中，它们之间并无密切相关性。有趣的是，UCA1抑制了miR-132在下调Lrrfip1表达和促进VSMC增殖方面的作用。因此，UCA1在动脉粥样硬化中表达下调，并可能通过调节miR-132/Lrrfip1轴来促进VSMC增殖。
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