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Cited by 5Chronic Obstructive Pulmonary Disease (COPD) ResearchMicroRNA in disease regulationPulmonary Hypertension Research and Treatments

MiR‐23a‐3p alleviates cigarette smoke extract‐induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema

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Li, Ke, Ye, Xianwei, Xu, Mei, Xu, Chuan, Lu, Ping, Li, Jiayi, Yuan, Guohang, Zhang, Cheng·2023·The Clinical Respiratory Journal
DOI 10.1111/crj.13707PMC PMC10730501
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Abstract

Background: 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. Methods: 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. Results: 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. Conclusion: MiR‐23a‐3p alleviated emphysema progression, which could inhibit CSE‐induced PMVECs apoptosis by targeting DNAJB1.

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  • miR-23a specifically binds to p53 to stimulate its transcriptional activity in cardiomyocytes and promotes oxidative stress-induced cell apoptosis.

    “it also specifically binds to p53 to stimulate its transcriptional activity in cardiomyocytes and promotes oxidative stress-induced cell apoptosis.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [60]

    The Discussion (page unavailable) reports the opposite effect in cardiomyocytes: miR-23a-3p overexpression alleviated high-glucose-induced apoptosis. The Results section on miR-23a-3p targeting (page unavailable) identifies DNAJB1, not p53; no passage supports p53 binding or stimulation of its transcriptional activity. (LLM, conf=0.88)

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  • In rats with myocardial ischemia-reperfusion injury, miR-23 can target FoxO3a to regulate cardiomyocyte growth, leading to increased cardiomyocyte apoptosis, while overexpression of miR-23 effectively reduced this phenomenon.

    “In rats with myocardial ischemia-reperfusion injury, it can target FoxO3a to regulate cardiomyocyte growth, leading to increased cardiomyocyte apoptosis while the overexpression of miR-23 effectively reduced this phenomenon [[60], [61], [62]].”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [60]

    The Discussion (page unavailable) reports that miR-23a-3p overexpression alleviated high-glucose-induced cardiomyocyte apoptosis. It does not support the claim’s rat myocardial ischemia-reperfusion setting, FoxO3a target, or regulation of cardiomyocyte growth; the paper’s Results instead identify DNAJB1 as the target in pulmonary vascular endothelial cells. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • miR-23a inhibits cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1, thus alleviating pulmonary emphysema development.

    “For instance, miR-23a inhibits cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1, thus alleviating pulmonary emphysema development;”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [60]

  • Overexpression of miR-23a-3p can promote cell viability and repress apoptosis.

    “Additionally, there are certain studies explicit that overexpression of miR-23a-3p can promote cell viability as well as repressed apoptosis.”

    From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [60]

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Cited by

Sorted by citations

Authors
Li, K., Ye, X., Xu, M., Xu, C., Lu, P., Li, J., Yuan, G., & Zhang, C.
Affiliations
Guizhou Provincial People's Hospital (CN)
Corresponding author
Zhang, Cheng
ORCID
Venue
The Clinical Respiratory Journal
Publisher
Wiley
Published
2023-10-12
Volume
17
Issue
12
Pages
1223-1232
ISSN
  • 1752-6981 (ISSN-L)
  • 1752-699X
DOI
10.1111/crj.13707
PMC
PMC10730501
OpenAlex
W4387598663
Cited by
5
References
1
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 1
FWCI
0.92
Type
journal article
Language
en
Open access
Licence
Locations
  • The Clinical Respiratory Journal (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Health Commission of Guizhou Province
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
Keywords
miR-23a-3p, DNAJB1, emphysema, cigarette smoke extract, pulmonary endothelial cells, apoptosis, microRNA, chronic obstructive pulmonary disease, lung injury, microRNA target regulation
MeSH terms
Cigarette Smoking, Animals, Emphysema, Humans, Pulmonary Emphysema, Apoptosis, MicroRNAs, Endothelial Cells, HSP40 Heat-Shock Proteins, Mice

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