miR144-3p inhibits PMVECs excessive proliferation in angiogenesis of hepatopulmonary syndrome via Tie2
Autor: | Bin Yi, Yihui Yang, Keyi Lv, Bin Chen, Kaizhi Lu, Xiangfa Ai, Hongfu Yu, Yong Yang, Congwen Yang |
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Rok vydání: | 2018 |
Předmět: |
Male
0301 basic medicine Angiogenesis Down-Regulation Rats Sprague-Dawley 03 medical and health sciences Downregulation and upregulation microRNA medicine Animals Hepatopulmonary syndrome Cells Cultured Cell Proliferation Neovascularization Pathologic biology Endothelial Cells Cell Biology Cell cycle medicine.disease Receptor TIE-2 Angiopoietin receptor Rats Up-Regulation Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Tyrosine kinase 2 Cell culture Cancer research biology.protein Hepatopulmonary Syndrome |
Zdroj: | Experimental Cell Research. 365:24-32 |
ISSN: | 0014-4827 |
Popis: | 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. |
Databáze: | OpenAIRE |
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