LPS Up-Regulates Cystathionine γ -Lyase Gene Expression in Primary Human Macrophages via NF-κB/ERK Pathway.

Alireza Badiei, S. Gieseg, S. Davies, Mohd Izani Othman, M. Bhatia
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引用次数: 22

Abstract

Hydrogen sulfide (H2S) is an endogenous inflammatory mediator produced by the activity of cystathionine γ-lyase (CSE) in mammals. Macrophages are a key element of the immune system and play a crucial role in inflammation. To determine the role of H2S and macrophages in inflammation, we investigated the expression of CSE in human primary macrophages. Our results show that H2S is produced by the activity of CSE in these cells. To investigate the role of common signalling pathway in biosynthesis of CSE in human primary macrophages, specific inhibitors were used to block NF-κB, ERK, p38 and JNK. Inhibition of NF-κB, ERK significantly reduced levels of CSE gene and protein expression in these cells but inhibition of JNK and p38 did not have an inhibitory effect on the expression of CSE gene in macrophages. Inhibition of NF-κB and ERK prevented the effect of LPS on H2S synthesizing activity in human primary macrophages. These data showed that H2S acts as an inflammatory mediator via NF-κB/ERK pathway in macrophages.
LPS通过NF-κB/ERK通路上调人巨噬细胞半胱硫氨酸γ -裂解酶基因表达。
硫化氢(H2S)是哺乳动物体内由半胱硫氨酸γ-裂解酶(CSE)活性产生的内源性炎症介质。巨噬细胞是免疫系统的重要组成部分,在炎症中起着至关重要的作用。为了确定H2S和巨噬细胞在炎症中的作用,我们研究了CSE在人原代巨噬细胞中的表达。我们的结果表明,在这些细胞中,H2S是由CSE的活性产生的。为了研究共同信号通路在人原代巨噬细胞CSE生物合成中的作用,我们使用特异性抑制剂阻断NF-κB、ERK、p38和JNK。抑制NF-κB、ERK可显著降低巨噬细胞中CSE基因表达水平和蛋白表达,而抑制JNK和p38对巨噬细胞中CSE基因表达无抑制作用。抑制NF-κB和ERK可阻止LPS对人原代巨噬细胞H2S合成活性的影响。这些数据表明H2S在巨噬细胞中通过NF-κB/ERK通路发挥炎症介质的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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