Evidence for microvesicle particles in UVB-mediated IL-8 generation in keratinocytes.

Shweta Bhadri, Pariksha Thapa, Yanfang Chen, Christine M Rapp, Jeffrey B Travers
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引用次数: 2

Abstract

Recent studies have implicated bioactive microvesicle particles (MVP) in the keratinocyte response to many environmental stressors, in partricular ultraviolet B radiation (UVB). The generation of MVP in response to UVB involves the Platelet-activating factor receptor (PAFR) and the enzyme acid sphingomyelinase (aSMase). As UVB generates some cytokines such as interleukin-8 (IL-8) in a PAFR-dependent manner, one question is if the production and release of IL-8 and MVP could be linked. Using the human keratinocyte-derived cell line HaCaT, the present in vitro studies indicate that pretreatment of HaCaT keratinocytes with PAFR agonist ester can synergize with low fluences of UVB to generate high levels of MVP as well as IL-8 protein. Treatment of cells with an aSMase pharmacologic inhibitor blocked both processes. These studies indicate the possibility that MVP could be involved in pathologic processes involving UVB-generated production of pro-inflammatory cytokines such as IL-8.

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微泡颗粒在uvb介导的角质形成细胞中产生IL-8的证据。
最近的研究表明,生物活性微泡颗粒(MVP)参与了角质形成细胞对许多环境应激源的反应,特别是紫外线B辐射(UVB)。针对UVB产生的MVP涉及血小板活化因子受体(PAFR)和酸性鞘磷脂酶(aSMase)。由于UVB以pafr依赖的方式产生一些细胞因子,如白细胞介素-8 (IL-8),因此IL-8的产生和释放是否与MVP有联系是一个问题。利用人角质形成细胞来源的HaCaT细胞系,目前的体外研究表明,PAFR激动剂酯预处理HaCaT角质形成细胞可以与低UVB作用协同产生高水平的MVP和IL-8蛋白。用aSMase药理学抑制剂处理细胞阻断了这两个过程。这些研究表明,MVP可能参与了uvb产生的促炎细胞因子(如IL-8)的病理过程。
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