Research Paper Volume 16, Issue 17 pp 12379—12391
Cigarette smoke-induced exosomal miR-221-3p facilitates M1 macrophage polarization via the STAT3 pathway in chronic obstructive pulmonary disease
- 1 Graduate School of Dalian Medical University, Dalian, China
- 2 Department of Respiratory and Critical Care Medicine, Central Hospital Affiliated to Shenyang Medical College, Shenyang, China
- 3 Department of Respiratory Medicine, Shengjing Hospital of China Medical University, Shenyang, China
Received: January 9, 2024 Accepted: July 23, 2024 Published: August 29, 2024
https://doi.org/10.18632/aging.206095How to Cite
Copyright: © 2024 Jia et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Aims: Chronic obstructive pulmonary disease (COPD) is marked by irreversible airflow limitations stemming from small airway constriction and lung emphysema. The advancement of COPD is greatly influenced by the M1 polarization of macrophages. The mechanisms governing macrophage polarization in inflammation conditions in COPD are not yet fully understood.
Methods: To investigate the interplay between exosomes triggered by cigarette smoke and the polarization of macrophages, we utilized a combination of flow cytometry, quantitative real-time reverse transcription PCR, and western blot analysis.
Results: Our research reveals that cigarette smoke (CS) exposure induces the secretion of exosomes from human bronchial epithelial cells, with exosomal miR-221-3p identified as a key player in modulating the polarization of M1 macrophages. The evidence indicates that cigarette smoke promotes exosome secretion in these cells, with exosomal miR-221-3p targeting SOCS3 and regulating the STAT3 signaling pathway to facilitate M1 macrophage polarization.
Conclusions: This research delves into the molecular pathways through which miR-221-3p facilitates the polarization of M1 macrophages, presenting a groundbreaking approach for potential targeted therapy in COPD.