TRANSFORMING GROWTH FACTOR-BETA(1) ENHANCES GLOMERULAR COLLAGEN-SYNTHESIS IN DIABETIC RATS
TRANSFORMING GROWTH FACTOR-BETA(1) ENHANCES GLOMERULAR COLLAGEN-SYNTHESIS IN DIABETIC RATS
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DOI：
10.2337/diabetes.42.11.1673
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发表时间：
1993-11-01
期刊：
影响因子：
7.7
通讯作者：
REDDI, AS
中科院分区：
文献类型：
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作者：
BOLLINENI, JS;REDDI, AS
在正常和糖尿病大鼠体外肾小球胶原合成及其对不同浓度的转化生长因子-β 1的反应进行了研究。TGF-β 1以剂量依赖性方式增加正常肾小球中胶原蛋白的合成，高达5 ng/ml。浓度>5 ng/ml显示胶原蛋白合成逐渐下降。基础胶原合成增加糖尿病肾小球，但添加TGF-β 1没有影响。TGF-β 1抗体阻止了胶原蛋白合成的增加。糖尿病大鼠循环TGF-β 1浓度及其mRNA表达均高于正常大鼠。虽然添加TGF-β 1并没有增加体外合成，但没有效果与其受体的下调一致，这归因于高循环水平。这项研究清楚地表明，TGF-β 1在正常大鼠肾小球胶原蛋白合成的调节作用，并提出了一个可能的因果关系，在糖尿病大鼠胶原蛋白合成增强的作用。
In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta1 were studied in normal and diabetic rats. TGF-beta1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. Concentrations >5 ng/ml showed a gradual decline in collagen synthesis. Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta1 had no effect. Antibody to TGF-beta1 prevented this increase in collagen synthesis. Both circulating TGF-beta1 concentration and its glomerular expression of mRNA were higher in diabetic than in normal rats. Although addition of TGF-beta1 did not increase synthesis in vitro, the absence of an effect is consistent with downregulation of its receptors attributable to the high circulating levels. This study clearly indicates a regulatory role of TGF-beta1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat.