Down-regulation of 1ncRNA MEG3 promotes hypoxia-induced human pulmonary artery smooth muscle cell proliferation and migration via repressing PTEN by sponging miR-21

Down-regulation of 1ncRNA MEG3 promotes hypoxia-induced human pulmonary artery smooth muscle cell proliferation and migration via repressing PTEN by sponging miR-21
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1ncRNA MEG3 的下调通过海绵 miR-21 抑制 PTEN 促进缺氧诱导的人肺动脉平滑肌细胞增殖和迁移

DOI:
10.1016/j.bbrc.2017.11.185
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发表时间:
2018-01-15
影响因子:
3.1
通讯作者:
Tang, Chengchun
Tang, Chengchun
中科院分区:
生物学4区
文献类型:
--
作者:
Zhu, Boqian;Gong, Yaoyao;Tang, Chengchun

文献摘要

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相似文献

缺氧性肺动脉高压是一种由于肺血管阻力进行性增加、肺血管不可逆重构并导致右心室衰竭而引起的危及生命的疾病。近年来的研究表明,肺动脉平滑肌细胞增殖和迁移在缺氧性肺动脉高压的发病机制中起重要作用。然而,缺氧性肺动脉高压的机制是复杂的,在很大程度上不清楚。本研究发现,缺氧条件下人肺动脉平滑肌细胞中IncRNA MEG 3表达下调,抑制MEG 3表达可促进正常和缺氧条件下的细胞增殖和迁移。进一步的研究表明MEG 3在正常和缺氧条件下均通过调节miR-21的表达发挥其功能。此外,我们展示了miR-21对PTEN的调节及其在缺氧中的作用。最终,我们的研究表明MEG 3在正常和缺氧条件下均通过miR-21/PTEN轴在人肺动脉平滑肌细胞中发挥作用。(C)2017由Elsevier Inc.出版
Hypoxia-induced pulmonary hypertension is a life-threatening disease arising from a progressive increase in pulmonary vascular resistance, irreversible pulmonary vascular remodeling and resulting in right ventricular failure. Recent studies suggested that pulmonary artery smooth muscle cell proliferation and migration played an important role in the pathogenesis of hypoxia-induced pulmonary hypertension. However, the mechanisms of hypoxia-induced pulmonary hypertension are complicated and largely unclear. In this study, we discovered that IncRNA MEG3 was down-regulated in human pulmonary artery smooth muscle cell in hypoxia, and inhibition of MEG3 promoted the cell proliferation and cell migration in both normal and hypoxia condition. Further study demonstrated that MEG3 exerted its function via regulation of miR-21 expression in both normal and hypoxia condition. In addition, we displayed the modulation of PTEN by miR-21 and their role in hypoxia. Ultimately, our study illustrated that MEG3 exerts its role via miR-21/PTEN axis in human pulmonary artery smooth muscle cell under both normal and hypoxia conditions. (C) 2017 Published by Elsevier Inc.