糖基化终产物对大鼠肾脏结缔组织生长因子的作用

被引：5

作者：

周桂华

李才

苗春生

机构：

[1] 吉林大学再生医学科学研究所病理研究室

[2] 吉林大学再生医学科学研究所病理研究室长春

[3] 长春

来源：

中华肾脏病杂志 | 2004年 / 03期

关键词：

糖基化终产物; 结缔组织生长因子; 糖尿病肾病; 转化生长因子-β;

D O I：

暂无

中图分类号：

R692 [肾疾病];

学科分类号：

1002 ; 100210 ;

摘要：

目的探讨糖基化终产物(AGEs)对大鼠肾脏结缔组织生长因子(CTGF)表达及细胞外基质(ECM)合成的影响。方法将Wistar大鼠随机分成4组:正常对照组(Con)、单纯大鼠血清蛋白组(RSP)、糖化血清组(AGEs)和氨基胍组(AG)。尾静脉注射AGE-RSP6周后,采用RT-PCR、免疫组织化学和蛋白质印迹杂交等方法检测AGEs对大鼠肾皮质TGF-β1和CTGF的mRNA和蛋白质表达及ECM蛋白成分表达的影响。结果与Con及RSP组比较,AGEs组肾小球系膜细胞增生,ECM红染区增大。AGEs组大鼠肾皮质TGF-β1和CTGF的mRNA和蛋白质表达均明显上调(P<0.01);TGF-β1和CTGF免疫组化阳性表达部位主要位于肾小球;肾小球ECM蛋白成分胶原(Col)Ⅳ和纤连蛋白(FN)合成也增多(P<0.05)。AG组上述所有变化均减轻。结论AGEs能明显诱导大鼠肾皮质CTGFmRNA和蛋白质表达增强,并使ECM蛋白成分合成增多。AGEs可能通过诱导CTGF表达上调引起ECM合成增多。

引用

页码：9 / 12

页数：4

共 10 条

[1]

AnimalmodelofscleroticskinI:localinjectionsofbleomycininducescleroticskinmimickingscleroderma. YamamotoT,,TakagawaS,KatayamaI,etal. JInvestDermatol . 1999

[2]

Stimulationof1fibroblastcellgrowth,matrixproduction,andgranulationtissueformationbyconnectivetissuegrowthfactor. FrazierK,WilliamsS,KothapalliD,etal. JInvestDermatol . 1996

[3]

Connective tissue growth factor mediates transforming growth factor beta induced collagen synthesis: down regulation by camp. Duncan MR,Frazier KS,Abramson S,et al. The FASEB Journal . 1999

[4]

Suppression subtractive hybridization identifies high glucose levels as a stimulus for expression of connective tissue growth factor and other genes in human mesangial cells. Murphy M,Godson C,Cannon S,et al. Journal of Biological Chemistry . 1999

[5]

Exogenous advanced glycosylation end products induce complex vascular dysfunction in normal animals: a model for diabetic and aging complications. Vlassara H,Fuh H,Makita Z, et al. Proceedings of the National Academy of Sciences of the United States of America . 1992

[6]

Renal connective tissue growth factor induction in experimental diabetes is prevented by aminoguanidine. Twigg SM,Cao Z,MCLennan SV,et al. The Journal of Endocrinology . 2002

[7]

PDGF and TGFbeta mediate collagen production by mesangial cells exposed to advanced glycosylation end products. Throckmorton DC,Brogden AP,Min B,et al. Kidney International . 1995

[8]

MessengerribonucleicacidsforMAC25andconnectivetissuegrowthfactor(CTGF)areinverselyregulatedduringfollicuulogenesisandearlyluteogenesis. WandjiSA,GadsbyJE,BarberJA,etal. The Journal of Endocrinology . 2000

[9]

Advancedglycosylationendproductsup-regulateconnectivetissuegrowthfactor(insulin-likegrowthfactor-bindingprotein2)inhumanfibroblasts:apotentialmechanismforexpressionofextracellularmatrixindiabetesmellitus. StephenM,MichelleM,AlisonH,etal. The Journal of Endocrinology . 2001

[10]

A novel transforming growth factor beta response element controls the expression of the connective tissue growth factor gene. Grotendorst GR,Okochi H,Hayashi-N. Cell Growth and Differentiation . 1996

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