Department of Anesthesiology and Pain Medicine, Kosin University College of Medicine, Busan, Korea.
Department of Anatomy, College of Medicine, Yeungnam University, Daegu, Korea.
J Cell Mol Med. 2020 Oct;24(20):12211-12218. doi: 10.1111/jcmm.15843. Epub 2020 Sep 15.
Although diesel airborne particulate matter (PM2.5) has been known to play a role in many human diseases, there is no direct evidence that therapeutic drugs or proteins can diminish PM2.5-induced diseases. Nevertheless, studies examining the negative control mechanisms of PM2.5-induced diseases are critical to develop novel therapeutic medications. In this study, the consensus PDZ peptide of ZO-1 inhibited PM2.5-induced inflammatory cell infiltration, pro-inflammatory cytokine gene expression, and TEER in bronchoalveolar lavage (BAL) fluid and AM cells. Our data indicated that the PDZ domain in ZO-1 is critical for regulation of the PM2.5-induced inflammatory microenvironment. Therefore, the PDZ peptide may be a potential therapeutic candidate during PM-induced respiratory diseases.
尽管柴油空气颗粒物（PM2.5）已被证实与许多人类疾病有关，但目前尚无直接证据表明治疗药物或蛋白质可以减轻 PM2.5 引起的疾病。然而，研究 PM2.5 引起的疾病的负性调控机制对于开发新型治疗药物至关重要。在这项研究中，ZO-1 的 PDZ 共识肽抑制了 PM2.5 诱导的炎症细胞浸润、促炎细胞因子基因表达以及支气管肺泡灌洗液（BAL）和 AM 细胞中的 TEER。我们的数据表明，ZO-1 中的 PDZ 结构域对于调节 PM2.5 诱导的炎症微环境至关重要。因此，PDZ 肽可能是 PM 诱导的呼吸道疾病治疗的潜在候选药物。
