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阻断Smad3表达对转化生长因子β1诱导肌成纤维细胞增殖的影响 被引量:9

Effects of siRNA-Smad3 on Growth of C2C12 Cells Induced by Transforming Growth Factor-β1
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摘要 目的探讨转化生长因子β1及其信号转导分子Smad3在肌成纤维细胞C2C12殖中的作用。方法以转化生长因子β1作用于C2C12细胞,对其信号转导分子Smad3基因进行RNA干扰,用MTT法检测转化生长因子β1诱导的C2C12细胞增殖。结果0、1、5和10μg/L转化生长因子β1作用C2C12细胞24h后,C2C12细胞增殖随转化生长因子β1浓度增加而增加,且呈剂量依赖性(光密度值分别为0.096±0.015、0.177±0.014、0.240±0.028和0.312±0.012,P<0.01);经200pmol/LsiRNA-Smad3转染24h后,再用5μg/L转化生长因子β1作用,其细胞增殖(光密度值0.063±0.011)比内对照组下降(光密度值0.137±0.016,P<0.01)。结论转化生长因子β1通过Smad3信号转导促进C2C12细胞增殖并呈剂量依赖性,siRNA-Smad3可有效阻断其信号转导而降低C2C12细胞增殖。 Aim To investigate the effects of Smad3 on the growth of C2C12 cells induced by transforming growth factor-β1 (TGF-β1 ). Methods C2C12 cells were transfected with siRNA-Smad3 in vitro, and the cell proliferations were examined with MTT methods. Results After the C2Cl2 cells interfered with different concentrations of TGF-131 (0, 1, 5, 10μg/L) for 24 h, the MTT (OD) values were 0.096± 0.015, 0.177±0.014, 0.240±0.028, 0.312±0.012 respectively (P〈0.01). While the C2C12 cells were transfected with 200 pmol/L siRNA-Smad3 for 24 h and then treated with 5 μg/L of 3GF-β1, the MTT ( OD ) values in experimental group ( 0. 063 ± 0.011 ) were decreased compared with internal control group ( 0.137 ± 0. 016, P 〈 0.01 ). Conelusion The TGF-β1 could promote C2Cl2 cells proliferation by the Smad3 pathway and showed dose dependent manner, siRNA-Smad3 could block the signal transduction and decreased C2Cl2 cell proliferation effectively.
出处 《中国动脉硬化杂志》 CAS CSCD 2008年第4期281-283,共3页 Chinese Journal of Arteriosclerosis
基金 湖南省卫生厅科研基金(B2005-072) 教育部留学回国启动基金(2006-331)
关键词 病理学与病理生理学 成纤维细胞 SMAD3基因 转化生长因子Β1 RNA干扰 Fibroblast Cell Smad3 Transforming Growth Factor-β1 RNA Interference
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  • 1杨彬,马颖哲,马岩,刘坤.基质金属蛋白酶与动脉粥样硬化[J].吉林大学学报(医学版),2004,30(5):831-834. 被引量:4
  • 2Franck Verrecchia,Alain Mauviel.Transforming growth factor-β and fibrosis[J].World Journal of Gastroenterology,2007,13(22):3056-3062. 被引量:114
  • 3Bobik A, Agrotis A, Kanellakis P, Dilley R, Krushinsky A, Smimov V, et al. Distioct patterns of transforming growth factor-β isoform and receptor experession in human atherosclerotic lesions: colocalization implicates TGF-β in fibrofatty lesion development [J]. Circulation, 1999, 99 (22): 2 883-891 被引量:1
  • 4Mallat Z, Tedgui A. The role of transfoming growth factor beta in atherosclerosis: novel insights and future perspectives [J]. Curr Opin Lipidol, 2002, 13(50) : 523-529 被引量:1
  • 5Lutgens E, Gijbel M, Smook M, De Muinck ED, Grewal IS, Koteliansky VE,et al. Transforming growth factor-beta mediates balance between inflammation. and fibrosis during plaque progression[ J ]. Arterioscler Thromb Vasc Biol,2002, 22 (6): 975-982 被引量:1
  • 6Reiner Z, Tedeschi-Reiner E. New information on the pathophysiology of atherosclerosis [J]. Lijec Vjesn, 2001, 123 (1-2): 26-31 被引量:1
  • 7Lutgens E, Gorelik L, Daemen MJ. De Muinck ED, Grewal IS. Koteliansky VE,et al. Both early and delayed anti-CD40L antibody treatment induce a stable plaque phenotype [J]. Proc Natl Acad Sci USA, 2000, 13:7464-469 被引量:1
  • 8Steen DK, Ravn HB, Falk E. Insight to the pathophysiology of instable coronary artery disease [J]. Am J Cardiol, 1997, 80(5A): 5E-9E 被引量:1
  • 9Mason DP, Kenagy RD, Hasenstab D, Bowen-Pope DF, Seifert RA, Coats S, et al. Matrix metalloproteinase-9 overexpression enhances vascular smooth muscle cell migration and alters remodeling in the injured rat carotid artery[ J ]. Circ Res, 1999, 85 (12): 1 179-185 被引量:1
  • 10Hong BK, Kwon HM, Lee BK, Kim D, Kim IJ, Kang SM, et al. Coexpression of cyclooxygenase-2 and matrix metalloproteinases in human aortic atherosclerotic lesions [J]. Yonsei Med J, 2000, 41 (1): 82-88 被引量:1

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