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.
出处
《上海交通大学学报（医学版）》
CAS
CSCD
北大核心
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)~~
