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首页> 外文期刊>American Journal of Physiology >Parathyroid hormone-related protein modulates inflammation in mouse mesangial cells and blunts apoptosis by enhancing COX-2 expression
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Parathyroid hormone-related protein modulates inflammation in mouse mesangial cells and blunts apoptosis by enhancing COX-2 expression

机译：甲状旁腺激素相关蛋白通过增强COX-2表达调节小鼠髓细胞中的炎症，并钝化细胞凋亡

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Injury of mesangial cells (MC) is a prominent feature of glomerulonephritis. Activated MC secrete inflammatory mediators that induce cell apoptosis. Parathyroid hormone-related peptide (PTHrP) is a locally active cytokine that enhances cell survival and is upregulated by proinflammatory factors in many cell types. The aim of this study was to analyze the regulation of PTHrP expression by inflammatory cytokines and to evaluate whether PTHrP itself acts as a proinflammatory and/or survival factor on male murine MC in primary culture. Our results showed that IL-1β (10 ng/ml) and TNF-a (10 ng/ml) rapidly and transiently upregulated PTHrP expression in MC. The effects of IL-1β were both transcrip-tional and posttranscriptional, with stabilization of the PTHrP mRNA by human antigen R (HuR). Proteome profiler arrays showed that PTHrP itself enhanced cytokines within 2 h in cell lysates, mainly IL-17, IL-16, IL-la, and IL-6. PTHrP also stimulated sustained expression (2-4 h) of chemokines, mainly regulated upon activation normal T cell expressed and secreted (RANTES)/C-C motif chemo-kine 5 (CCL5) and macrophage inflammatory protein-2 (MIP-2)/C-X-C motif chemokine 2 (CXCL2), thymus and activation-regulated chemokine (TARC)/CCL17, and interferon-inducible T cell a-che-moattractant (I-TAC)/CXCL11. Moreover, PTHrP markedly enhanced cyclooxygenase-2 (COX-2) expression and elicited its auto-induction through the activation of the NF-kB pathway. PTHrP induced MC survival via the COX-2 products, and PTHrP overex-pression in MC blunted the apoptotic effects of IL-1(3 and TNF-a. Altogether, these findings suggest that PTHrP functions as a booster of glomerular inflammatory processes and may be a negative feedback loop preserving MC survival.
机译：Mesangial细胞损伤（MC）是肾小球肾炎的突出特征。活化MC分泌诱导细胞凋亡的炎症介质。甲状旁腺激素相关的肽（PPTHP）是一种局部活性细胞因子，可增强细胞存活，并通过许多细胞类型的促炎因子上调。本研究的目的是分析炎症细胞因子的PTHRP表达的调节，并评估PTHRP本身是否作为初级培养物中雄性鼠MC上的促炎和/或存活因子。我们的结果表明，IL-1β（10ng / ml）和TNF-A（10ng / mL）在MC中快速且瞬时上调的PTHRP表达。 IL-1β的效果是转录和术语，通过人抗原R（HUR）稳定PTHRP mRNA。蛋白质组分布器阵列显示PTHRP本身在细胞裂解物中的2小时内增强细胞因子，主要是IL-17，IL-16，IL-LA和IL-6。 PTHRP还刺激了趋化因子的持续表达（2-4小时），主要调节在激活正常T细胞上表达和分泌的（RANTES）/ CC基序化学 - Kine 5（CCL5）和巨噬细胞炎症蛋白-2（MIP-2）/ CXC主题趋化因子2（CXCL2），胸腺和活化调节的趋化因子（TARC）/ CCL17，以及干扰素诱导的T细胞A-Che-MoAttractant（I-TAC）/ CXCL11。此外，PTHRP明显增强了环氧氧酶-2（COX-2）的表达，并引发了通过NF-KB途径的活化引发的自身诱导。 PPThp通过Cox-2产品诱导MC存活，MC中的PTHRP过度压力钝化IL-1（3和TNF-A.完全，这些发现表明PTHRP用作肾小球炎症过程的增强剂是保留MC生存的负面反馈回路。

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