间充质干细胞条件培养基对炎症介导的肺动脉血管平滑肌细胞增殖调控的研究  

Regulation of Mesenchymal Stem Cell Conditioned Medium on Proliferation of Pulmonary Artery Smooth Muscle Cells Mediated by Inflammation

作　　者：牛志浩[1] 刘庆[2] 刘俊峰[1,3] 吴西军[3,4] 何志旭 NIU Zhihao;LIU Qing;LIU Junfeng;WU Xijun;HE Zhixu(Clinical Laboratory,North China Petroleum General Administration Hospital,Renqiu 062552,Hebei,China;Department of Respiratory and Critical Care Medicine,Affiliated Hospital of Guizhou Medical University,Gu,iyang 550004,Guizhou,China;Tissue Engineering and Stern Cell Researeh Center,Guizhou Medical University,Guiyang 550004,Guizhou,China;Department of immunology,Guizhou Medical University,Guiyang 550004,Guizhou,China;Department of Child Blood Oncology,Affiliated Hosptial of Guizhou Medical University,Guiyang 550004,Guizhou,China)

机构地区：[1]华北石油管理局总医院检验科,河北任丘062552 [2]贵州医科大学附院呼吸与危重症医学科,贵州贵阳550004 [3]贵州医科大学组织工程与干细胞实验中心,贵州贵阳550004 [4]贵州医科大学免疫学教研室,贵州贵阳550004 [5]贵州医科大学附院儿童血液肿瘤科,贵州贵阳550004

出　　处：《贵州医科大学学报》2018年第6期641-645,共5页Journal of Guizhou Medical University

基　　金：国家自然科学基金项目(30560159);贵州省"125计划"重大科技专项[黔教合重大专项字(2013)021];贵阳市-贵州医科大学联合科技计划项目[筑科合同(20151001)03]

摘　　要：目的:探讨间充质干细胞条件培养基(MSC-CM)对炎症介导的肺动脉血管平滑肌细胞(PASMC)增殖的调控机制。方法:取4~6代处于对数生长期人脐带MSC,建立体外细胞培养体系,分为对照组(PASMC)、T淋巴细胞刺激组(PASMC+T淋巴细胞)、MSC-CM干预组(PMSMC+T淋巴细胞+MSC-CM);分别于培养第3天时,检测3组培养上清中肿瘤坏死因子(TNF)-α含量、PASMC的增殖、钙调神经磷酸酶(Ca N)活性及活化的T淋巴细胞核因子2(NFATc2)活化情况。结果:与T淋巴细胞刺激组比较,MSC-CM干预组TNF-α的生成显著减少(P<0.01);与对照组和T淋巴细胞刺激组比较,MSC-CM干预组的PASMC内Ca N的磷酸酶活性降低、NFATc2的活化减少,PASMC的增殖降低(P<0.01)。结论:MSC-CM可能通过Ca N/NFAT信号通路抑制炎症介导的PASMC增殖。Objective： To investigate the regulatory mechanism of Mesenchymal Stem Cell conditioned medium（ MSC-CM） on proliferation of pulmonary artery smooth muscle cells（ PASMC） mediated by inflammation. Methods： In vitro cell culture system was established by taking MSC from human umbilical cord at logarithmic growth stage and divided into control group（ PASMC）,T lymphocyte stimulation group（ PASMC ＋ T lymphocyte） and MSC-CM intervention group（ PASMC ＋ T lymphocyte＋ MSC-CM）. On the third day of culture,the levels of tumor necrosis factor（ TNF）-α in culture supernatant,proliferation of PASMC,Ca N activity and activated NFATc2 were assessed. Results： The production of TNF-α in MSC-CM intervention group was significantly lower than that in T-lymphocyte stimulation group（ P〈0. 01）. Compared with control group and T lymphocyte stimulation group,the activity of Ca N phosphatase in PASMC of MSC-CM intervention group was decreased,activation of NFATc2 was reduced,and the proliferation of PASMC was reduced（ P〈0. 01）. Conclusion： MSCCM inhibits the proliferation of PASMC mediated by inflammation through the Ca N/NFAT signaling pathway.

关 键 词：间充质干细胞 肺动脉高压 平滑肌 增殖 肿瘤坏死因子-Α T淋巴细胞核因子2 钙调神经磷酸酶 

分 类 号：R456[医药卫生—治疗学]