miRl44-3p inhibits PMVECs excessive proliferation in angiogenesis of hepatopulmonary syndrome via Tie2
miRl44-3p inhibits PMVECs excessive proliferation in angiogenesis of hepatopulmonary syndrome via Tie2
复制标题
miRl44-3p通过Tie2抑制肝肺综合征血管生成中PMVEC过度增殖
DOI：
10.1016/j.yexcr.2018.02.009
复制
发表时间：
2018-04-01
影响因子：
3.7
通讯作者：
Lu, Kaizhi
中科院分区：
文献类型：
--
作者：
Yang, Congwen;Lv, Keyi;Lu, Kaizhi
背景/目的：越来越多的证据表明microRNAs（miRNAs）与肝病综合征（HPS）相关。本研究旨在探讨miR-144在HPS血管生成中的作用及其机制。方法：检测HPS大鼠肺微血管内皮细胞（PMVECs）和肺组织中miR-144- 3 p的表达水平。我们预测了miR-144- 3 p的潜在靶点。酪氨酸激酶2（Tyrosine kinase 2，Tie 2）是miR 144 - 3 p的靶基因，在肺血管新生中起重要作用。此外，检查了miR-144- 3 p调节对Tie 2的影响。结果：miR-144- 3 p在HPS组织和细胞系中表达下调，过表达miR-144 - 3 p可显著抑制PMVEC的增殖和细胞周期。结论：miR-144 - 3 p可通过Tie 2的表达负调控PMVEC的增殖。此外，miR-144- 3 p的过表达可能证明作为HPS治疗的治疗策略是有益的。
Background/aim: Increasing evidence show microRNAs (miRNAs) are associated with hepatopulmonary syndrome (HPS). The aim of this study was to investigate the role of miR-144 in the angiogenesis of HPS, as well as to identify its underlying mechanism.Methods: The expression levels of miR-144-3p were assessed in pulmonary micro-vascular endothelial cells (PMVECs), as well as in lung tissues from rats with HPS. We predicted the potential target of miR-144-3p. Tyrosine kinase 2(Tie2) was identified as a target gene of miR144-3p, which has an essential role in the angiogenesis of lung vessel. In addition, the effects of miR-144-3p regulated on Tie2 was examined. The upregulation and down-regulation of miR-144-3p can affect the proliferation of PMVECs.Results: We found that the levels of miR-144-3p were frequently downregulated in HPS tissues and cell lines, and overexpression of miR-144-3p dramatically inhibited PMVECs proliferation and cell cycle. We further verified the Tie2 as a novel and direct target of miR-144-3p in HPS.Conclusion: miR-144-3p can negatively regulate PMVECs proliferation by Tie2 expression. In addition, over expression of miR-144-3p may prove beneficial as a therapeutic strategy for HPS treatment.