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首页> 美国卫生研究院文献>Environmental Health Perspectives >Transcription factor activation following exposure of an intact lung preparation to metallic particulate matter.
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Transcription factor activation following exposure of an intact lung preparation to metallic particulate matter.

机译：将完整的肺部制剂暴露于金属颗粒物质后转录因子激活。

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Metallic constituents contained in ambient particulate matter have been associated with adverse effects in a number of epidemiologic, in vitro, and in vivo studies. Residual oil fly ash (ROFA) is a metallic by-product of the combustion of fossil fuel oil, which has been shown to induce a variety of proinflammatory responses in lung cells. We have examined signaling pathways activated in response to ROFA exposure and recently reported that ROFA treatment activates multiple mitogen-activated protein (MAP) kinases in the rat lung. In the present study we extended our investigations on the mechanism of toxicity of ROFA to include transcription factors whose activities are regulated by MAP kinases as well as possible effectors of transcriptional changes that mediate the effects of ROFA. We applied immunohistochemical methods to detect ROFA-induced activation of nuclear factor-kappa B (NF kappa B), activating transcription factor-2 (ATF-2), c-Jun, and cAMP response element binding protein (CREB) in intact lung tissue and confirmed and characterized their functional activation using DNA binding assays. We performed these studies using a perfused rabbit lung model that is devoid of blood elements in order to distinguish between intrinsic lung cell effects and effects that are secondary to inflammatory cell influx. We report here that exposure to ROFA results in a rapid activation of all of the transcription factors studied by exerting direct effects on lung cells. These findings validate the use of immunohistochemistry to detect transcription factor activation in vivo and demonstrate the utility of studying signaling changes in response to environmental exposures.
机译：在许多流行病学，体外和体内研究中，环境颗粒物所含的金属成分均与不良反应有关。残留的粉煤灰（ROFA）是化石燃料油燃烧的金属副产物，已证明可诱导肺细胞发生多种促炎反应。我们已经检查了响应ROFA暴露而激活的信号通路，最近报道了ROFA治疗可以激活大鼠肺中的多种促分裂原活化蛋白（MAP）激酶。在本研究中，我们扩展了对ROFA毒性机制的研究，包括其活性受MAP激酶调节的转录因子以及可能介导ROFA的转录变化的效应子。我们应用免疫组化方法检测了完整肺组织中ROFA诱导的核因子-κB（NF kappa B），转录因子2（ATF-2），c-Jun和cAMP反应元件结合蛋白（CREB）的激活并使用DNA结合测定法确认并表征了其功能激活。我们使用没有血液成分的灌注兔肺模型进行了这些研究，以区分内在的肺细胞影响和继发于炎性细胞流入的影响。我们在这里报告，暴露于ROFA会导致对肺细胞产生直接影响的所有转录因子快速激活。这些发现验证了免疫组织化学在体内检测转录因子激活的用途，并证明了研究信号响应环境暴露变化的实用性。

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