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作 者:林绍慧[1] 盛净[1] 马绍骏[1] 陆平[1] 蔡文玮[1] 胡萍[1]
机构地区:[1]上海交通大学医学院附属第九人民医院老年科,上海200011
出 处:《上海交通大学学报(医学版)》2014年第3期274-278,共5页Journal of Shanghai Jiao tong University:Medical Science
基 金:上海市科委基金(10JC1408902)~~
摘 要:目的探讨C1q肿瘤坏死因子相关蛋白3(CTRP3)对转化生长因子β1(TGF-β1)诱导的血管外膜成纤维细胞(AFs)增殖以及α-平滑肌肌动蛋白(α-SMA)表达的调节作用。方法采用细胞贴壁法培养SD大鼠胸主动脉AFs;CCK-8检测不同浓度CTRP3(0.1、1、10和50μg/mL)对AFs增殖的影响;免疫荧光、Real-Time PCR和Western blotting检测CTRP3对AFsα-SMA表达的影响。结果 CTRP3可呈剂量依赖性抑制TGF-β1诱导的AFs增殖,随着浓度升高,其抑制能力增强,浓度为10μg/mL时,其对AFs增殖的抑制作用最强(P<0.01);免疫荧光、Real-Time PCR和Western blotting结果显示,CTRP3可明显抑制TGF-β1诱导的α-SMA mRNA和蛋白表达(P<0.01)。结论 CTRP3可在体外抑制TGF-β1诱导AFs的增殖和α-SMA表达,提示其潜在的改善病理性血管重构作用。Objective To investigate the effects of Clq/TNF-related protein-3 (CTRP3) on transforming growth factor-β1 (TGF--β1) induced proliferation and expression of a-smooth muscle actin (α-SMA) among adventitial fibroblasts (AFs). Methods AFs were isolated from thoracic aortas of male Sprague Dawly (SD) rats. The ceils in passage 3 to 5 were treated with various concentrations of CTRP3 (0. 1, 1, 10, 50 txg/mL). The effects of CTRP3 on proliferation of AFs were examined by Cell Counting Kit (CCK-8). Immunoflueresence assay, Real-Time PCR, and Western blotting were adopted to detect the expression of a-SMA of AFs. Results CTRP3 attenuated the proliferative activities induced by TGF-β1 in a dose-dependent manner, and the most marked effect could be observed at the concentration of 10 μg/mL (P 〈 0. 01). Immunoflueresence assay, Real-Time PCR and Western blotting showed that CTRP3 could significantly inhibited TGF-β1 induced upregulation of a-SMA both at the mRNA and protein levels (P 〈 0.01). Conclusion CTRP3 has significant inhibition effects on proliferation and a-SMA expression of adventitial fibroblasts induced by TGF-β1, which suggests the potential value of CTRP3 in the treatment of pathological vascular remodeling.
关 键 词:血管外膜成纤维细胞 C1 q肿瘤坏死因子相关蛋白 3 转化生长因子β1 Α-平滑肌肌动蛋白 增殖
分 类 号:R543[医药卫生—心血管疾病]
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