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p38 MAPK mediates high glucose-induced renal tubular epithelial-mesenchymal transition
Author(s): 
Pages: 759-766
Year: Issue:  6
Journal: Acta Physiologica Sinica

Keyword:  p38MAPK上皮细胞向间充细胞转变Snaill糖尿病肾病大鼠;
Abstract: 本文旨在观察p38 MAPK与高糖诱导的肾小管上皮细胞向间充质细胞转变之间的关系.将雄性Sprague-Dawley(SD)大鼠随机分为对照组、糖尿病组、胰岛素治疗组,用免疫组织化学、Western blot检测p38 MAPK和磷酸化p38 MAPK(p-p38 MAPK)蛋白表达.采用机械分离和酶消化获取SD大鼠肾小管节段,进行肾小管上皮细胞培养,将肾小管上皮细胞分为对照组、高渗组(20 mmol/L D-mannitol)、高糖组(20 mmol/L D-glucose)和SB202190(p38 MAPK特异性抑制剂)+高糖组,处理72 h后收集细胞,用免疫细胞化学检测a-平滑肌肌动蛋白(a-smooth muscle actin,a-SMA)、p-p38 MAPK和Snail1 蛋白表达,Western blot检测p38 MAPK、p-p38 MAPK、Snaill、转化生长因子β1(transforming growth factor-β1,TGF-β1)、a-SMA和E-cadherin的表达,RT-PCR检测a-SMA和E-cadherin mRNA的表达.体内和体外结果均显示,高糖状态激活了p38 MAPK,这种活化作用在体内可因胰岛素控制血糖而被消除,在体外可被p38 MAPK特异性抑制剂SB202190显著抑制:高糖组a-SMA蛋白和mRNA在原代培养.肾小管上皮细胞的表达较对照组分别增加12倍和8倍(P<0.01),SB202190处理组其表达则较高糖组分别减少67%和50%(P<0.01).SB202190不影响TGF-β1蛋白表达,但下调Snaill蛋白表达,并部分恢复高糖组E-cadherin蛋白和mRNA的表达.上述结果提示,p38 MAPK可能通过转录因子Snaill介导高糖诱导的肾小管上皮细胞向间充质细胞转变.
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