• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >The involvement of phosphatidylinositol 3-kinase /Akt signaling in high glucose-induced downregulation of GLUT-1 expression in ARPE cells
【24h】

The involvement of phosphatidylinositol 3-kinase /Akt signaling in high glucose-induced downregulation of GLUT-1 expression in ARPE cells

机译：磷脂酰肌醇3-激酶/ Akt信号通路参与高糖诱导的ARPE细胞中GLUT-1表达的下调

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Glucose transporters have been reported to be associated with the development of diabetic retinopathy. Retinal pigment epithelial cells (RPEs) are believed to play an important role in the pathogenesis of diabetic retinopathy. However, the effect of hyperglycemia on glucose transporters in RPEs and the related signal pathways have not yet been elucidated. Therefore, we examined the effect of high glucose on the glucose transporter 1 in ARPEs and the related signal molecules. In the present study, high glucose decreased 2-deoxyglucose uptake in a time (>2 h) and dose dependent manner. In addition, we found that high glucose downregulated the expression of glucose transporter 1 (GLUT-1). The high glucose-induced downregulation of GLUT-1 was blocked by Wortmanin, LY 294002 (PI-3 kinase inhibitors) and Akt (Akt inhibitor). The high glucose increased stimulation of Akt activation in a time dependent manner. We also investigated the upstream regulator of Akt activation. The high glucose-induced phosphorylation of Akt was blocked by bisindolymaleimide I, H-7, staurosporine (protein kinase C [PKC] inhibitors), vitamin C and catalase (antioxidants). In addition, the high glucose-induced downregulation of GLUT-1 was also blocked by PKC inhibitors and antioxidants. Moreover, high glucose increased lipid peroxide formation, which was prevented by PKC inhibitors. In conclusion, high glucose downregulated GLUT-1 by Akt pathway activation mediated by the PKC-oxidative stress signaling pathway in ARPE cells. 500Diabetic retinopathy; Retinal pigment epithelial cells; PT-3 kinase/Akt; Protein kinase C
机译：据报道，葡萄糖转运蛋白与糖尿病性视网膜病的发展有关。视网膜色素上皮细胞（RPE）被认为在糖尿病性视网膜病的发病机理中起着重要作用。然而，尚未阐明高血糖对RPE中葡萄糖转运蛋白的作用和相关的信号通路。因此，我们研究了高葡萄糖对ARPEs中葡萄糖转运蛋白1和相关信号分子的影响。在本研究中，高葡萄糖以一定的时间（> 2 h）和剂量依赖性方式降低了2-脱氧葡萄糖的摄取。此外，我们发现高糖下调了葡萄糖转运蛋白1（GLUT-1）的表达。 Wortmanin，LY 294002（PI-3激酶抑制剂）和Akt（Akt抑制剂）阻止了高葡萄糖诱导的GLUT-1的下调。高葡萄糖以时间依赖性方式增加了对Akt激活的刺激。我们还研究了Akt激活的上游调节剂。高糖诱导的Akt磷酸化被双吲哚马来酰亚胺I，H-7，星形孢菌素（蛋白激酶C [PKC]抑制剂），维生素C和过氧化氢酶（抗氧化剂）阻断。此外，PKC抑制剂和抗氧化剂也阻止了高葡萄糖诱导的GLUT-1的下调。此外，高葡萄糖增加了脂质过氧化物的形成，这被PKC抑制剂阻止。总之，高糖通过ARPE细胞中PKC-氧化应激信号转导途径介导的Akt途径激活来下调GLUT-1。 500糖尿病性视网膜病;视网膜色素上皮细胞; PT-3激酶/ Akt;蛋白激酶C

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号