南方医科大学学报2016，Vol.36Issue(10)：1322-1327,6.DOI:10.3969/j.issn.1673-4254.2016.10.04
乌司他丁通过上调PPAR-γ抑制低氧诱导的肺血管平滑肌细胞表型转换
Ulinastatin inhibits hypoxia-induced phenotype modulation of pulmonary artery smooth muscle cells by up-regulating PPAR-γexpression
摘要
Abstract
Objective To evaluate the effect of ulinastatin on hypoxia-induced phenotype modulation of pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. Method Cultured PASMCs from SD rats were exposed to normoxic condition, normoxia with ulinastatin treatment, hypoxia, or hypoxia with ulinastatin treatment. After 24 h of exposures, the cells were examined for SM-α-actin and caplonin expressions with immunofluorescence assay and for cell migration with CCK-8 and H-TdR assays. Western blotting was used for detecting the expressions of PPAR-γin the cells, and PPAR-γ-responsive firefly luciferase reporter was employed for measuring the transcriptional activity of PPAR-γ. The PPAR-γinhibitor GW9662 was used to explore the mechanism of the inhibitory effect of ulinastatin on hypoxia induced-phenotype modulation of PASMCs by measuring the changes in cell proliferation and migration. Results Ulinastatin obviously enhanced the expressions of SM-α-actin and calponin (P<0.05), inhibited the proliferation and migration (P<0.05), and up-regulated the expression of PPAR-γin PASMCs exposed to hypoxia (P<0.05). Pretreatment of the cells with GW9662 abolished the effect of ulinastatin on hypoxia-induced phenotype modulation of PASMCs and enhanced the cell proliferation and migration (P<0.05). Conclusion Ulinastatin inhibits hypoxia-induced phenotype modulation of PASMCs from rats possibly by up-regulating the expression of PPAR-γ.关键词
乌司他丁/低氧/平滑肌细胞/表型转换/细胞增殖/细胞运动Key words
ulinstatin/hypoxia/pulmonary artery smooth muscle cells/phenotype modulation/cell proliferation/cell movement引用本文复制引用
唐锟,刘畅,陈林,高静,张超..乌司他丁通过上调PPAR-γ抑制低氧诱导的肺血管平滑肌细胞表型转换[J].南方医科大学学报,2016,36(10):1322-1327,6.基金项目
国家自然科学基金（81170053） Supported by National Natural Science Foundation of China (81170053) （81170053）
