相扑蛋白
基因敲除
生物
缺氧诱导因子
细胞生物学
细胞生长
缺氧(环境)
细胞周期
小发夹RNA
血管内皮生长因子
细胞
癌症研究
分子生物学
细胞凋亡
泛素
化学
生物化学
基因
有机化学
氧气
血管内皮生长因子受体
作者
Fang Zhou,Aiguo Dai,Yong-Liang Jiang,Xiao Tan,Xiufeng Zhang
出处
期刊:Molecular Medicine Reports
[Spandidos Publications]
日期:2016-03-03
卷期号:13 (4): 3482-3490
被引量:16
标识
DOI:10.3892/mmr.2016.4969
摘要
Hypoxic pulmonary vascular remodeling (HPSR) has an important role in the development of hypoxic pulmonary hypertension. HPSR is predominantly mediated by the proliferation of pulmonary artery smooth muscle cells (PASMCs). Our previous study demonstrated that hypoxia‑inducible factor (HIF)‑1α was able to promote the proliferation of PASMCs. Small ubiquitin‑like modifier (SUMO)ylation is a post‑translational modification that is important in various cellular processes. It has previously been demonstrated that HIF‑1α may be SUMOylated by SUMO. Conversely, SUMO‑specific protease 1 (SENP‑1) was able to increase the stability of HIF‑1α by decreasing SUMOylation of HIF‑1α. In order to investigate whether SUMOylation of HIF‑1α has a role in the proliferation of PASMCs, the present study cultured PASMCs in hypoxic and normoxic chambers in vitro. The proliferation ability of PASMCs was measured using the Cell Counting kit‑8 and 5‑ethynyl‑2'‑deoxyuridine cell proliferation assays. In addition, short hairpin RNA lentiviral particles were used to knockdown the expression of SENP‑1, and the expression levels of HIF‑1α, SENP‑1 and vascular endothelial growth factor (VEGF) were detected at the mRNA and protein levels using semi‑quantitative polymerase chain reaction and western blotting, respectively. The present study demonstrated that SENP‑1 was able to enhance the proliferative ability of PASMCs by initiating deSUMOylation of HIF‑1α and increasing the expression of its downstream responsive gene, VEGF.
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