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首页> 美国政府科技报告 >Sulfur Mustard Induced Cytokine Production and Cell Death: Investigating the Potential Roles of the p38, p53, and NF-kappaB Signaling Pathways with RNA Interference
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Sulfur Mustard Induced Cytokine Production and Cell Death: Investigating the Potential Roles of the p38, p53, and NF-kappaB Signaling Pathways with RNA Interference

机译：硫芥诱导细胞因子产生和细胞死亡：研究p38，p53和NF-κB信号通路与RNa干扰的潜在作用

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摘要

Cutaneous and ocular injuries caused by sulfur mustard (SM; bis-(2- chloroethyl) sulfide) are characterized by severe inflammation and death of exposed cells. Given the known roles of p38MAPK and NF-kappaB in inflammatory cytokine production, and the known roles of NF-kappaB and p53 in cell fate, these pathways are of particular interest in the study of SM injury. In this study, we utilized inhibitory RNA (RNAi) targeted against p38 , the p50 subunit of NF-kappaB, or p53 to characterize their role in SM-induced inflammation and cell death in normal human epidermal keratinocytes (NHEK). Analysis of culture supernatant from 200 muM SM-exposed cells showed that inflammatory cytokine production was inhibited by p38 RNAi but not by NF-kappaB p50 RNAi. These findings further support a critical role for p38 in SM-induced inflammatory cytokine production in NHEK and suggest that NF-kappaB may not play a role in the SM-induced inflammatory response of this cell type. Inhibition of NF-kappB by p50 RNAi did, however, partially inhibit SM-induced cell death, suggesting a role for NF-kappaB in SM-induced apoptosis or necrosis. Interestingly, inhibition of p53 by RNAi potentiated SM-induced cell death, suggesting that the role of p53 in SM injury, may be complex and not simply prodeath.

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