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首页> 外文期刊>Cellular Physiology and Biochemistry >mPGES-1-Derived PGE2 Contributes to Indoxyl Sulfate-Induced Mesangial Cell Proliferation
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mPGES-1-Derived PGE2 Contributes to Indoxyl Sulfate-Induced Mesangial Cell Proliferation

机译：mPGES-1衍生的PGE2有助于硫酸吲哚酚诱导的系膜细胞增殖。

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>Background/Aims: We previously reported that indoxyl sulfate (IS) could cause mesangial cell (MC) proliferation via a cyclooxygenase (COX)-2-dependent mechanism. However, the specific prostaglandin contributing to COX-2 effect on IS-induced MC proliferation remained unknown. Thus, the present study was undertaken to examine the role of microsomal prostaglandin E synthase-1 (mPGES-1)-derived Prostaglandin E2 (PGE2) in IS-induced MC proliferation. Methods: IS was administered to the MCs with or without mPGES-1 siRNA pretreatment to induce the MC proliferation which was determined by cell cycle analysis, DNA synthesis, and the expressions of cyclins. In another experimental setting, PGE2 was applied to the MCs to examine its direct effect on MC proliferation, as well as the regulation of prostaglandin E receptors (EPs) by qRT-PCR. Results: With the administration of IS, mPGES-1(not mPGES-2 and cytosolic PGES) was significantly upregulated at both protein and mRNA levels in line with a promoted MC proliferation. Interestingly, silencing mPGES-1 reduced cell number in S and G2 phases and blocked the upregulation of cyclin A2 and cyclin D1 in parallel with blunted PGE2 release after IS treatment, indicating that mPGES-1-derived PGE2 could contribute to MC proliferation. Furthermore, we confirmed that exogenous PGE2 could directly trigger the proliferative response in MCs. Lastly, we observed a selective upregulation of EP2 after PGE2 treatment and enhanced phosphorylation of NF-?oB following IS administration in MCs, suggesting the potential involvements of EP2 and NF-?oB in this pathological process. Conclusion: mPGES-1-derived PGE2 contributed to IS-induced mesangial cell proliferation.
机译：> 背景/目的： 我们以前曾报道过，硫酸吲哚酚（IS）可能通过依赖于环氧合酶（COX）-2的机制引起系膜细胞（MC）增殖。但是，尚不清楚对COX-2对IS诱导的MC增殖有影响的特定前列腺素。因此，本研究旨在探讨微粒体前列腺素E合酶1（mPGES-1）衍生的前列腺素E2（PGE 2 ）在IS诱导的MC增殖中的作用。 方法： 将IS进行MCs预处理，并进行mPGES-1 siRNA预处理，以诱导MC增殖，这是通过细胞周期分析，DNA合成以及siRNA的表达来确定的。细胞周期蛋白。在另一个实验环境中，将PGE 2 应用于MC，以检查其对MC增殖的直接影响以及qRT-PCR对前列腺素E受体（EPs）的调节。 结果： 施用IS后，mPGES-1（不是mPGES-2和胞质PGES）在蛋白质和mRNA水平上均显着上调，这与MC增殖促进一致。有趣的是，沉默mPGES-1可以减少S和G2期的细胞数量，并在IS处理后与钝化的PGE 2 释放同时阻止细胞周期蛋白A2和细胞周期蛋白D1的上调，表明mPGES-1衍生的PGE 2 可能促进MC增殖。此外，我们证实外源性PGE 2 可以直接触发MCs的增殖反应。最后，我们观察到PGE2处理后EP2的选择性上调和在MC中IS给药后NF-αoB磷酸化的增强，提示EP2和NF-αoB可能参与了这种病理过程。 结论： mPGES-1衍生的PGE 2 有助于IS诱导的系膜细胞增殖。

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