期刊文献+

CTGF反义寡核苷酸对高糖培养人肾小球系膜细胞细胞外基质表达的影响 被引量:3

原文传递
导出
摘要 目的:观察体外转染结缔组织生长因子(CTGF)反义寡核苷酸(ASODN)对高糖培养的人肾小球系膜细胞(HMC)细胞外基质表达的影响。方法:体外培养HMC,予以高糖(30mmol/L)和正常糖(5mmol/L)培养液培养,高糖培养后应用脂质体Lipofectamine2000转染CTGFASODN,在不同时间收集培养液上清。用ELISA检测培养液上清中的纤连蛋白(FN)和层黏连蛋白(LN)含量。结果:高糖呈时间依赖促进体外培养的HMC表达FN和LN,而转染CTGFASODN可抑制高糖所致的FN和LN分泌增加。结论:高糖培养可促进HMC细胞外基质的表达,转染CTGFASODN可抑制上述高糖的作用。故调控HMC的CTGF表达水平可能成为防治糖尿病肾病(DN)、特别是早期病变的有效途径之一。
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2009年第6期556-558,共3页 Chinese Journal of Cellular and Molecular Immunology
基金 辽宁省教育厅科学研究项目(202013140) 辽宁省自然科学基金资助项目(20032068)
  • 相关文献

参考文献6

  • 1Mason RM,Wahab NA.Extracellular matrix metabolismin diabetic nephropathy[J].Am Soc Nephrol,2003,14(5):1358-1373.
  • 2Vasylyeva TL,Ferry RG.Novel roles of the IGF-IGFBPaxis in etiopathophysiology of diabetic nephropathy[J].Endocrinology,2007,76(2):177-186.
  • 3赵龙,邓红,汪颖南,苏宁,刘必成,刘东风.高糖、茶多酚对人系膜细胞结缔组织生长因子、纤维连接蛋白mRNA表达的影响[J].南京医科大学学报(自然科学版),2005,25(3):157-160. 被引量:5
  • 4Riser BL,Cortes P.Connective tissue growth factor and its regulation:a new element in diabetic glomerulosclerosis[J].Ren Fail,2001,23(3):459-470.
  • 5Schena FP,Gesualdo L.Pathogenetic mechanisms of diabetic nephropathy[J].Am Soc Nephrol,2005,16 (Suppl 1):S30-33.
  • 6Twigg SM,Chen MM,Joly AH,et al.Advanced glycosylation and products up-regulate connective tissue growth factor (insulinlike growth factor-binding protein-related protein 2)in human fibroblast apotential mechanism for expansion of extracellular matrix indiabetes mellitus[J].Endocrinology,2001,142(5):1760-1769.

二级参考文献24

  • 1Kikuchi K, Kadono T, Ihn H, et al. Growth regulation in scleroderma fibroblasts: increased response to transforming growth factor-beta 1 [J]. J Invest Dermatol,1995,105(1):128-132.
  • 2Torffvit O, Agardh CD. The impact of metabolic and blood pressure control on incidence and progression of nephropathy, A 10-year study of 385 type 2 diabetic patients [J ]. J Diabetes Complications, 2001,15: 307-313.
  • 3Wahab NA, Yevdokimova N, Weston BS. Role of connective tissue growth factor in the pathogenesis of diabetic nephropathy [ J ]. Biochem J, 2001,359: 77-87.
  • 4Lal MA, Korner A, Matsuo Y, et al. Combined antioxidant and COMT inhibitor treatnent reverses renal abnormalities in diabetic rats [J]. Diabetes, 2000, 49:1381-1389.
  • 5Suzuki S, Hinokio Y, Komatu K, et al. Oxidative damage to mitochondrial DNA and its relationship to diabetic complications [J]. Diabetes Res Clin Pract, 1999, 45:161-168.
  • 6Davison GW, George L, Jackson SK, et al. Exercise, free radicals, and lipid peroxidation in type 1 diabetes mellitus[J]. Free Radic Biol Med, 2002, 33: 1543-1551.
  • 7Ito Y, Aten J, Bende RJ, et al. Expression of connective tissue growth factor in human renal fibrosis [J]. Kidney Int, 1998, 53:853-861.
  • 8Heusinger-Ribeiro J, Eberlein M, Wahab NA, et al.Expression of connective tissue growth factor in human renal fibroblasts: regulatory roles of RhoA and cAMP[J].J Am Soc Nephrol, 2001, 12:1853-1861.
  • 9Wang S, Denichilo M, Brubaker C, et al. Connective tissue growth factor in tubulointerstitial injury of diabetic nephropathy[J]. Kidney Int, 2001, 60: 96-105.
  • 10Murphy M, Godson C, Cannon S, et al. Suppression subtractive hybridization identifies high glucose levels as a stimulus for expression of connective tissue growth factor and other genes in human mesangial cells [J]. J Biol Chem, 1999, 274:5830-5834.

共引文献4

同被引文献29

引证文献3

二级引证文献26

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部