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首页> 外文期刊>Molecular and Cellular Endocrinology >The function of miR-199a-5p/Klotho regulating TLR4/NF-kappa B p65/NGAL pathways in rat mesangial cells cultured with high glucose and the mechanism
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The function of miR-199a-5p/Klotho regulating TLR4/NF-kappa B p65/NGAL pathways in rat mesangial cells cultured with high glucose and the mechanism

机译：高糖培养大鼠系膜细胞中miR-199a-5p / Klotho调节TLR4 /NF-κBp65 / NGAL通路的功能及其机制

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摘要

Anti-aging protein Klotho may confer a renal protective effect via attenuating the nuclear factor-kappa B (NF-kappa B) p65 pathways activity. Besides, miR-199a-5p can promote gastric cancer by inhibition of Klotho protein expression. But little is known regarding to the role of miR-199a-5p/Klotho in regulating NF-kappa B p65 pathways in the pathogenesis of diabetic kidney disease (DKD). Thus, we explored Klotho and miR-199a-5p in terms of Toll-like receptor-4 (TLR4)/NF-kappa B p65eutrophil gelatinase associated lipocalin (NGAL) signaling pathways in high glucose cultured mesangial cells (MCs). We found that high glucose increased miR-199a-5p expression, accompanied by the significantly decreased Klotho expression at both mRNA and protein. High glucose also activated TLR4/NF-kappa B p65/NGAL signaling pathways and promoted the downstream fibrosis and inflammatory reaction. Additionally, inhibition of miR-199a-5p or exogenous addition of Klotho restrained the activity of TLR4/NF-kappa B p65/NGAL signaling pathways, which in turn suppressed the inflammation and fibrosis in high glucose cultured MCs. This study provides a new basis to elucidate the protection mechanism of anti-aging protein Klotho in diabetic kidney. For the first time, our study prompts that miR-199a-5p can be used as a new therapeutic targets for DKD. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
机译：抗衰老蛋白Klotho可能通过减弱核因子-κB（NF-κB）p65途径的活性而赋予肾脏保护作用。此外，miR-199a-5p可以通过抑制Klotho蛋白表达来促进胃癌。但是，关于miR-199a-5p / Klotho在糖尿病肾病（DKD）发病机理中调控NF-κBp65途径的作用还知之甚少。因此，我们在高葡萄糖培养的系膜细胞（MCs）中，研究了Toll样受体4（TLR4）/NF-κBp65 /中性粒细胞明胶酶相关的脂钙素（NGAL）信号通路中的Klotho和miR-199a-5p。我们发现高糖增加了miR-199a-5p的表达，同时在mRNA和蛋白质上均显着降低了Klotho的表达。高葡萄糖还激活了TLR4 /NF-κBp65 / NGAL信号通路，并促进了下游纤维化和炎症反应。另外，抑制miR-199a-5p或外源添加Klotho抑制了TLR4 /NF-κBp65 / NGAL信号通路的活性，进而抑制了高糖培养的MCs的炎症和纤维化。该研究为阐明抗衰老蛋白Klotho在糖尿病肾中的保护机制提供了新的依据。我们的研究首次提示miR-199a-5p可用作DKD的新治疗靶标。 （C）2015 Elsevier Ireland Ltd.保留所有权利。

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