ArticleThe clinical respiratory journal2023
MiR-23a-3p alleviates cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema.
Article in The clinical respiratory journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Bone Marrow Stem Cell Exosomes Protect Lung Cells from Oxygen Damage by Regulating miR-23a-3p/Slc7a2 Pathway.The journal of gene medicine · 2026Article
- Recent advances of miR-23 in human diseases and growth development.Non-coding RNA research · 2025Review
- ER Stress-Related Biomarkers in Chronic Obstructive Pulmonary Disease: A Comprehensive Transcriptome, Mendelian Randomization, and Machine-Learning Analysis.International journal of chronic obstructive pulmonary disease · 2025Article
- Macrophage extracellular vesicle-packaged miR-23a-3p impairs maintenance and angiogenic capacity of human endothelial progenitor cells in neonatal hyperoxia-induced lung injury.Stem cell research & therapy · 2024Article
- MiR-23a-3p alleviates cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema.The clinical respiratory journal · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCigarette 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.
methodsCS 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.
resultsMiR-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.
conclusionMiR-23a-3p alleviated emphysema progression, which could inhibit CSE-induced PMVECs apoptosis by targeting DNAJB1.
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