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首页> 外文期刊>Alcohol >Malondialdehyde-acetaldehyde (MAA) adducted proteins bind to scavenger receptor A in airway epithelial cells
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Malondialdehyde-acetaldehyde (MAA) adducted proteins bind to scavenger receptor A in airway epithelial cells

机译：丙二醛-乙醛（MAA）加成蛋白与气道上皮细胞中的清道夫受体A结合

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Co-exposure to cigarette smoke and ethanol generates malondialdehyde and acetaldehyde, which can subsequently lead to the formation of aldehyde-adducted proteins. We have previously shown that exposure of bronchial epithelial cells to malondialdehyde-acetaldehyde (MAA) adducted protein increases protein kinase C (PKC) activity and proinflammatory cytokine release. A specific ligand to scavenger receptor A (SRA), fucoidan, blocks this effect. We hypothesized that MAA-adducted protein binds to bronchial epithelial cells via SRA. Human bronchial epithelial cells (BEAS-2B) were exposed to MAA-adducted protein (either bovine serum albumin [BSA-MAA] or surfactant protein D [SPD-MAA]) and SRA examined using confocal microscopy, fluorescent activated cell sorting (FACS), and immunoprecipitation. Differentiated mouse tracheal epithelial cells (MTEC) cultured by air-liquid interface were assayed for MAA-stimulated PKC activity and keratinocyte-derived chemokine (KC) release. Specific cell surface membrane dye co-localized with upregulated SRA after exposure to MAA for 3-7 min and subsided by 20 min. Likewise, MAA-adducted protein co-localized to SRA from 3 to 7 min with a subsequent internalization of MAA by 10 min. These results were confirmed using FACS analysis and revealed a reduced mean fluorescence of SRA after 3 min. Furthermore, increased amounts of MAA-adducted protein could be detected by Western blot in immunoprecipitated SRA samples after 3 min treatment with MAA. MAA stimulated PKCε-mediated KC release in wild type, but not SRA knockout mice. These data demonstrate that aldehyde-adducted proteins in the lungs rapidly bind to SRA and internalize this receptor prior to the MAA-adducted protein stimulation of PKC-dependent inflammatory cytokine release in airway epithelium.
机译：共同接触香烟烟雾和乙醇会生成丙二醛和乙醛，随后可导致醛加成蛋白的形成。以前我们已经表明，支气管上皮细胞暴露于丙二醛-乙醛（MAA）加成的蛋白质会增加蛋白激酶C（PKC）活性和促炎细胞因子的释放。清道夫受体A（SRA）的特定配体岩藻依聚糖可阻止此作用。我们假设MAA加成的蛋白通过SRA与支气管上皮细胞结合。将人支气管上皮细胞（BEAS-2B）暴露于MAA加成蛋白（牛血清白蛋白[BSA-MAA]或表面活性剂蛋白D [SPD-MAA]），并使用共聚焦显微镜，荧光激活细胞分选（FACS）检查SRA和免疫沉淀。通过气液界面培养的分化的小鼠气管上皮细胞（MTEC）测定了MAA刺激的PKC活性和角质形成细胞的趋化因子（KC）释放。暴露于MAA 3-7分钟并在20分钟内消退后，特定的细胞表面膜染料与上调的SRA共定位。同样，MAA加成的蛋白质在3至7分钟内共定位于SRA，随后在10分钟内将MAA内在化。这些结果通过FACS分析得到证实，并显示3分钟后SRA的平均荧光降低。此外，用MAA处理3分钟后，免疫沉淀的SRA样品中的蛋白质印迹可检测到增加量的MAA加成蛋白。 MAA刺激野生型，但不是SRA基因敲除小鼠的PKCε介导的KC释放。这些数据表明，在MAA加成蛋白刺激气道上皮中PKC依赖性炎性细胞因子释放之前，肺中醛加成蛋白会快速结合至SRA并使其内在化。

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