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- W4387598663 abstract "Cigarette smoke (CS) is an important risk factor for chronic obstructive pulmonary disease, including emphysema. MicroRNAs (miRNAs) are important regulators of emphysema progression. However, miR-23a-3p role in emphysema is unclear.CS exposure was used to construct emphysema mice models, and cigarette smoke extract (CSE)-induced pulmonary vascular endothelial cells (PMVECs) were used to mimic emphysema cell models. Mouse lung tissue was stained by immunohistochemical staining, hematoxylin and eosin staining, and TUNEL staining. MiR-23a-3p and DnaJ homolog subfamily B member 1 (DNAJB1) levels were tested using quantitative real-time PCR. DNAJB1 and apoptosis-related markers' protein levels were examined via western blot analysis. Cell viability and apoptosis were analyzed by MTT assay and flow cytometry. The interaction between miR-23a-3p and DNAJB1 was evaluated by dual-luciferase reporter assay and RIP assay.MiR-23a-3p was downregulated, and DNAJB1 was upregulated in CS-induced emphysema mice models and CSE-induced PMVECs. MiR-23a-3p overexpression promoted viability and repressed apoptosis in CSE-induced PMVECs. MiR-23a-3p targeted DNAJB1 and negatively regulated DNAJB1 expression. Moreover, DNAJB1 knockdown repressed CSE-induced PMVECs apoptosis, and miR-23a-3p inhibitor reversed this effect. Additionally, miR-23a-3p alleviated lung tissue injury and improved emphysema in mice by reducing DNAJB1 expression.MiR-23a-3p alleviated emphysema progression, which could inhibit CSE-induced PMVECs apoptosis by targeting DNAJB1." @default.
- W4387598663 created "2023-10-14" @default.
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- W4387598663 date "2023-10-12" @default.
- W4387598663 modified "2023-10-14" @default.
- W4387598663 title "MiR‐23a‐3p alleviates cigarette smoke extract‐induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema" @default.
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- W4387598663 doi "https://doi.org/10.1111/crj.13707" @default.
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