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首页> 外文期刊>Cell biology international. >Critical role of PBEF expression in pulmonary cell inflammation and permeability.
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Critical role of PBEF expression in pulmonary cell inflammation and permeability.

机译：PBEF表达在肺细胞炎症和通透性中的关键作用。

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Previous studies in our lab have identified pre-B-cell colony enhancing factor (PBEF) as a novel biomarker in acute lung injury. This study continues to elucidate the underlying molecular mechanism of PBEF in the pathogenesis of acute lung injury in pulmonary cell culture models. Our results revealed that IL-1beta induced PBEF expression in pulmonary vascular endothelial cells at the transcriptional level and a -1535 T-variant in the human PBEF gene promoter significantly attenuated its binding to an IL-1beta-induced unknown transcription factor. This may underlie the reduced expression of PBEF and thus the lower susceptibility to acute lung injury in -1535T carriers. Furthermore, overexpression of PBEF significantly augmented IL-8 secretion and mRNA expression by more than 6-fold and 2-fold in A549 cells and HPAEC, respectively. It also significantly augmented IL-1beta-mediated cell permeability by 44% in A549 cells and 65% in endothelial cells. The knockdown of PBEF expression significantly inhibitedIL-1beta-stimulated IL-8 secretion and mRNA level by 60% and 70%, respectively, and the knockdown of PBEF expression also significantly attenuated IL-1beta-induced cell permeability by 29% in epithelial cells and 24% in endothelial cells. PBEF expression also affected the expression of two other inflammatory cytokines (IL-16 and CCR3 genes). These results suggest that PBEF is critically involved in pulmonary vascular and epithelial inflammation and permeability, which are hallmark features in the pathogenesis of acute lung injury. This study lends further support to our finding that PBEF is a potential new target in acute lung injury.
机译：我们实验室中的先前研究已将B细胞集落增强因子（PBEF）作为急性肺损伤的新型生物标志物。这项研究继续阐明在肺细胞培养模型中PBEF在急性肺损伤的发病机理中的潜在分子机制。我们的结果表明，IL-1β诱导肺血管内皮细胞在转录水平上的PBEF表达，而人PBEF基因启动子中的-1535 T变体显着减弱了其与IL-1β诱导的未知转录因子的结合。这可能是PBEF的表达降低以及因此在-1535T携带者中对急性肺损伤的敏感性降低的基础。此外，PBEF的过表达在A549细胞和HPAEC中分别显着增强IL-8分泌和mRNA表达超过6倍和2倍。在A549细胞中，IL-1β介导的细胞通透性也显着提高了44％，在内皮细胞中也显着提高了65％。敲低PBEF表达可分别显着抑制IL-1beta刺激的IL-8分泌和mRNA水平60％和70％，敲低PBEF表达也可显着减弱IL-1beta诱导的上皮细胞和细胞的通透性29％。内皮细胞中占24％。 PBEF的表达还影响其他两种炎性细胞因子（IL-16和CCR3基因）的表达。这些结果表明PBEF关键参与肺血管和上皮的炎症和通透性，这是急性肺损伤的发病机制中的标志性特征。这项研究进一步支持了我们的发现，即PBEF是急性肺损伤的潜在新靶标。

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