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首页> 外文期刊>Journal of biochemical and molecular toxicology >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：硫芥子油诱导细胞因子的产生和细胞死亡：研究p38，p53和NF-kappaB信号通路在RNA干扰中的潜在作用。

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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 alpha, 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 microM SM-exposed cells showed that inflammatory cytokine production was inhibited by p38 alpha 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-kappaB 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.
机译：硫芥子气（SM;双-（2-氯乙基）硫化物）引起的皮肤和眼部损伤的特征是严重的炎症和裸露的细胞死亡。考虑到p38MAPK和NF-kappaB在炎症性细胞因子产生中的已知作用，以及NF-kappaB和p53在细胞命运中的已知作用，这些途径在SM损伤研究中尤为重要。在这项研究中，我们利用针对p38 alpha，NF-κB的p50亚基或p53的抑制性RNA（RNAi）来表征其在正常人表皮角质形成细胞（NHEK）中SM诱导的炎症和细胞死亡中的作用。对来自200 microM SM暴露细胞的培养上清液的分析表明，炎性细胞因子的产生受p38αRNAi抑制，但不受NF-κBp50 RNAi抑制。这些发现进一步支持了p38在NHEK中SM诱导的炎症细胞因子产生中的关键作用，并提示NF-κB可能在这种细胞类型的SM诱导的炎症反应中不起作用。然而，p50 RNAi抑制NF-kappaB确实部分抑制了SM诱导的细胞死亡，表明NF-kappaB在SM诱导的细胞凋亡或坏死中起作用。有趣的是，RNAi对p53的抑制作用增强了SM诱导的细胞死亡，这表明p53在SM损伤中的作用可能很复杂，而不仅仅是死亡。

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