MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
Introduction Bronchial epithelial cell damage is an important determinant of the severity of chronic obstructive pulmonary (COPD). However, the exact molecular mechanisms underlying this cell death in COPD development are not well understood. This study investigates the involvement of microRNA-21 (m...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2025-03-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | https://www.tobaccoinduceddiseases.org/MicroRNA-21-plays-a-role-in-exacerbating-chronic-obstructive-pulmonary-disease-by,202182,0,2.html |
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| Summary: | Introduction
Bronchial epithelial cell damage is an important determinant of the
severity of chronic obstructive pulmonary (COPD). However, the exact molecular
mechanisms underlying this cell death in COPD development are not well
understood. This study investigates the involvement of microRNA-21 (miR-21/
miRNA-21) in COPD and its underlying molecular mechanism.
Methods
A mouse model of COPD was created by exposing the mice to cigarette
smoke (CS) and injecting them with cigarette smoke extract (CSE). Both wildtype
mice and miR-21 knockout (miR-21-/-) mice were used to investigate
the role of microRNA-21 (miR-21) in exacerbating COPD. Various assays and
analyses were performed, including HE staining, tunel staining, enzyme-linked
immunosorbent assay (ELISA), flow cytometry, quantitative real-time polymerase
chain reaction (RT-qPCR), and western blotting (WB) to measure outcomes such
as the pathological morphological changes, necroptosis, apoptosis, and levels of
inflammatory factors.
Results
Our results revealed an upregulation of miR-21 in the lung tissue of
COPD model mice. Additionally, knockout of miR-21 resulted in decreased
levels of bronchial epithelial cell necroptosis and apoptosis, as evidenced by the
downregulation of tumor necrosis factor receptor 1 (TNFR1), phosphoryl-mixed
lineage kinase domain-like protein (p-MLKL) and caspase-3. This downregulation
of necroptosis and apoptosis ultimately led to a reduction of inflammatory factors
and damage-associated molecular patterns (DAMPs), such as tumor necrosis
factor-α (TNF-α), interleukin-1β (IL- 1β), and interleukin-6 (IL-6) and high
mobility group protein B1(HMGB1) in the lungs, thereby ameliorating COPD.
Conclusions
Our findings suggest that miR-21 contributes to the worsening of
chronic obstructive pulmonary disease by modulating necroptosis and apoptosis
in bronchial epithelial cells, providing a new theoretical basis for the pathogenesis
of chronic obstructive pulmonary disease. |
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| ISSN: | 1617-9625 |