Congwen Yang1, Keyi Lv2, Bin Chen1, Yong Yang1, Xiangfa Ai1, Hongfu Yu1, Yihui Yang1, Bin Yi3, Kaizhi Lu4. 1. Department of Anesthesiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China. 2. Department of Developmental Neuropsychology, School of Psychology, Third Military Medical University, Chongqing 400038, China. 3. Department of Anesthesiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China. Electronic address: yibin1974@163.com. 4. Department of Anesthesiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China. Electronic address: lukaizhi2010@163.com.
Abstract
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, overexpression of miR-144-3p may prove beneficial as a therapeutic strategy for HPS treatment.
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, overexpression of miR-144-3p may prove beneficial as a therapeutic strategy for HPS treatment.
Authors: Lin Chen; Yi Han; Yujie Li; Bing Chen; Xuehong Bai; Karine Belguise; Xiaobo Wang; Yang Chen; Bin Yi; Kaizhi Lu Journal: Cell Death Dis Date: 2019-11-07 Impact factor: 8.469