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...

Full description

Saved in:
Bibliographic Details
Main Authors: Zhengpeng Zeng, Xuelian Liu, Fei Xiang, Xue He, Jiahui Li, Hanying Liu, Lihua Xie
Format: Article
Language:English
Published: European Publishing 2025-03-01
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
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850173993897689088
author Zhengpeng Zeng
Xuelian Liu
Fei Xiang
Xue He
Jiahui Li
Hanying Liu
Lihua Xie
author_facet Zhengpeng Zeng
Xuelian Liu
Fei Xiang
Xue He
Jiahui Li
Hanying Liu
Lihua Xie
author_sort Zhengpeng Zeng
collection DOAJ
description 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.
format Article
id doaj-art-1bfb078db83a4ff5ad19036e06964b6a
institution OA Journals
issn 1617-9625
language English
publishDate 2025-03-01
publisher European Publishing
record_format Article
series Tobacco Induced Diseases
spelling doaj-art-1bfb078db83a4ff5ad19036e06964b6a2025-08-20T02:19:44ZengEuropean PublishingTobacco Induced Diseases1617-96252025-03-0123March1910.18332/tid/202182202182MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cellsZhengpeng Zeng0https://orcid.org/0009-0002-5172-2508Xuelian Liu1Fei Xiang2Xue He3Jiahui Li4Hanying Liu5Lihua Xie6Health Management Medicine Center, The Third Xiangya Hospital, Central South University, Changsha, ChinaHealth Management Medicine Center, The Third Xiangya Hospital, Central South University, Changsha, ChinaRespiratory and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha, ChinaHealth Management Medicine Center, The Third Xiangya Hospital, Central South University, Changsha, ChinaChangsha Kexin Cancer Hospital, Changsha, ChinaHealth Management Medicine Center, The Third Xiangya Hospital, Central South University, Changsha, ChinaRespiratory and Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha, ChinaIntroduction 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.https://www.tobaccoinduceddiseases.org/MicroRNA-21-plays-a-role-in-exacerbating-chronic-obstructive-pulmonary-disease-by,202182,0,2.htmlcigarette smokenecroptosisapoptosismicrorna-21chronic obstructive pulmonary
spellingShingle Zhengpeng Zeng
Xuelian Liu
Fei Xiang
Xue He
Jiahui Li
Hanying Liu
Lihua Xie
MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
Tobacco Induced Diseases
cigarette smoke
necroptosis
apoptosis
microrna-21
chronic obstructive pulmonary
title MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
title_full MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
title_fullStr MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
title_full_unstemmed MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
title_short MicroRNA-21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
title_sort microrna 21 plays a role in exacerbating chronic obstructive pulmonary disease by regulating necroptosis and apoptosis in bronchial epithelial cells
topic cigarette smoke
necroptosis
apoptosis
microrna-21
chronic obstructive pulmonary
url https://www.tobaccoinduceddiseases.org/MicroRNA-21-plays-a-role-in-exacerbating-chronic-obstructive-pulmonary-disease-by,202182,0,2.html
work_keys_str_mv AT zhengpengzeng microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells
AT xuelianliu microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells
AT feixiang microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells
AT xuehe microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells
AT jiahuili microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells
AT hanyingliu microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells
AT lihuaxie microrna21playsaroleinexacerbatingchronicobstructivepulmonarydiseasebyregulatingnecroptosisandapoptosisinbronchialepithelialcells