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( Hye-ryeon Heo ),( Young-youl Kim ),( Hyun Joung Lim ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Background Increasing researches have been reported that 8-hydroxydeoxyguanosine (8-OHdG), one of the wastes of DNA damages arising from oxidative stress, involved in ameliorating pathological exacerbation of in vitro and in vivo various disease models induced by damageable triggers. However, the action of the molecule in normal human bronchial epithelial cell line (BEAS- 2B) exposed to cadmium (Cd) has not been elucidated. In the current study, we investigated whether exogenous 8-OHdG contributes to alleviate pulmotoxicity when exposed to Cd in BEAS-2B cells. Methods We conducted real-time quantitative PCR (qPCR), H2DCFDA assay, flow cytometric analysis and immunoblots to identify the therapeutic effects of 8-OHdG on BEAS-2B cells exposed to Cd in terms of pathological changes, which are inflammatory response, ROS production, ER stress- and EMT-related gene expressions. Results 8-OHdG induced the down-regulation of inflammatory mediators in BEAS-2B cells exposed to Cd in RNA level and/or secretion forms. BEAS-2B cells treated with Cd and 8-OHdG accounted for the fewer cell population of color changes to green than cells just exposed to Cd, indicating that 8-OHdG diminishes intracellular ROS production in BEAS-2B cells exposed to Cd. 8-OHdG reduced the expressions of ER stress-related genes such as Bip, IRE1α and Ero1-Lα, and Fibronectin, Claudin, Snail1 and Slug related to EMT. Interestingly, recovery of E-cadherin expression was partially observed in BEAS-2B treated with Cd 10 μM and 8-OHdG. Conclusions 8-OHdG decreases pathological damages of BEAS-2B exposed to Cd by mitigating activations of inflammation, ROS, ER stress and EMT in transcriptional and translational levels. Taken together, these findings provide a basis that 8-OHdG can be a therapeutic candidate to attenuate continually vicious cycles inducing pathological injury (This work was supported by the Research Program funded by the Korea Disease Control and Prevention Agency(2020-NG-010-01)).
( Eun-sook Park ),( Hye-ryeon Heo ),( Ji-hye Jang ),( Young-youl Kim ),( Hyun Joung Lim ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Background Inhaled PM2.5 could induce adverse health effects in respiratory systems, but the underlying mechanisms are not well defined. We aim to explore the intrinsic mechanisms and new therapeutic targets regulating the PM2.5- exposed pathological conditions. Methods We performed a transciptomic analysis of cells isolated from PM2.5 (NIST 1650b) exposed 3D mucociliary tissues model (EpiAirway FT), in order to identify PM2.5-dependent mRNA and miRNA expression changes. Results A number of genes, miRNAs, biological process, KEGG pathways were identified during PM2.5 exposure in 3D mucociliary tissues. Compared with control DMSO group, we identified 779 upregulated or downregulated genes in PM2.5 exposed 3D EpiAirway groups. The top functions impacted by these gene expression changes included regulation of epithelial cilium movement, cilium-dependent cell motility and cilia structure. With respect to miRNA changes, we found that 23 targets were significantly changed and particularly identified 6 targets associated cilium. Using paired mRNA/miRNA-sequencing data, we found that targets gene and miRNAs can affect abnormal cilia motility. Conclusions This study suggests that PM2.5-induce changes in gene/miRNA expression may contribute to mucociliary clearance dysfunction via defects in cilia structure and function. And these changed target gene and miRNAs may contribute to the adverse respiratory effect of air pollution exposure (This work was supported by the Research Program funded by the Korea Disease Control and Prevention Agency (2020-NI-099-02)).