S100A4/Mts1在低氧诱导肺动脉平滑肌增殖中的作用机制  

Mechanism of S100A4/Mtsl in pulmonary arterial smooth muscle cells under hypoxia

作　　者：李运成[1] 刘婷[1] 贺斌峰[1] 王关嵩[1] 

机构地区：[1]第三军医大学新桥医院全军呼吸内科研究所军队及重庆市呼吸疾病重点实验室,重庆400037

出　　处：《中华肺部疾病杂志（电子版）》2012年第5期18-20,25,共4页Chinese Journal of Lung Diseases(Electronic Edition)

基　　金：国家自然科学基金(30971309)

摘　　要：目的探讨S100A4/Mtsl在低氧诱导肺动脉平滑肌增殖中的作用机制。方法大鼠肺动脉平滑肌细胞(PASMCs)分为对低氧刺激组及AG490干预组;免疫荧光分别检测常氧组、低氧刺激组及AG490干预组RPASMCs细胞S100A4/Mtsl的表达情况,Westernblot分别检测三组细胞的S100A4/Mtsl、p-JAK2、p-STAT3蛋白表达。结果低氧0hS100A4/Mtsl在胞浆中极少表达,低氧刺激后胞浆及胞核中明显表达;S100A4/Mtsl、p-JAK2、p-STAT3蛋白在低氧刺激8h比低氧刺激0h表达明显升高(P<0.05),AG490干预低氧刺激8h组三种蛋白的表达较低氧刺激8h组显著下降(P<0.05)。结论低氧刺激下S100A4/Mtsl基因在PAMSCs增殖中发挥重要作用,并且可被AG490抑制。Objective To investigate the the mechanism of S100A4/Mts1 in pulmonary arterial smooth muscle cells （PASMCs） under hypoxia. Methods PASMCs were divided into normoxic group, hypoxic group and an AG490 plus hypoxic group （AG490）. The immunofluorescence method was used to detect the expression of the S100A4/Mts1 in normoxic group and hypoxic group. Western blot was performed to examine the expression of S100A4/Mts1 protein, phospho-JAK2 protein and phospho-STAT3 protein in normoxic group, hypoxic group and an AG490 plus hypoxic group respectively. Results Immunofluorescence assay showed few expression of the S100A4/Mts1 in cytoplasm of PASMC in normoxic group, and significant expression in cytoplasm and nucleus of PASMC in hypoxic group; S100A4/Mts1 protein, phospho- JAK2 protein, phospho-STAT3 protein in 8 h hypoxic group was significantly higher than that in normoxic group （ P 〈 0.05 ） and they declined significantly in AG490 group as compared to 8 h hypoxic group. Conclusion S100A4/Mts1 gene plays important role in PAMSC proliferation induced by hpoxia, and could be blocked by AG490.

关 键 词：低氧 肺动脉平滑肌细胞 S100A4/Mts1 JAK-STAT 

分 类 号：R363[医药卫生—病理学]