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Published on: July 12, 2024
MicroRNA-382-5p is involved in pulmonary inflammation induced by fine particulate matter exposure
Xinwei Zhang1, Yanshu Zhang2, Qingtao Meng1
1Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, 210009, China.
Abstract:
Exposure to atmospheric particulate matter (PM) has been related to the increasing incidence and mortality of pulmonary diseases, where microRNAs (miRNAs) play significant roles in these biological and pathological processes. In the present study, we found that miR-382-5p played an anti-inflammatory role in pulmonary inflammation induced by fine particulate matter (PM2.5) or diesel exhaust particles (DEPs) in vitro and in vivo. The expression level of miR-382-5p was downregulated, while its target gene, namely CXCL12, was elevated in HBE cells after exposure to PM2.5 or DEPs. Mechanistically, PM2.5 or DEPs exposure increased CXCL12/MMP9 expression via miR-382-5p inhibition, subsequently triggered pulmonary inflammation. Furthermore, antagonizing the function of CXCL12 significantly reduced the expression of MMP9 and local inflammation induced by PM2.5 or DEPs. PM2.5 or DEPs caused apoptosis and G1 phase arrest could be partially restored by overexpression of miR-382-5p and antagonism of CXCL12. In a murine model, enhanced miR-382-5p expression effectively reduced expression levels of CXCL12, MMP9 and inflammatory cytokines, hereby protected lung tissues against PM2.5 or DEPs-induced lesions. Collectively, the miR-382-5p/CXCL12/MMP9 pathway may provide a mechanism, which mediates inflammatory response to PM2.5 or DEPs exposure.
Insights
MicroRNA-382-5p (miR-382-5p) combats pulmonary inflammation caused by fine particulate matter (PM2.5) and diesel exhaust particles (DEPs). This study reveals miR-382-5p protects lung tissues by targeting the CXCL12/MMP9 pathway.
Area of Science:
- Environmental Health
- Molecular Biology
- Pulmonology
Background:
- Particulate matter (PM) exposure is linked to increased pulmonary disease incidence and mortality.
- MicroRNAs (miRNAs) are key regulators in biological and pathological processes, including lung inflammation.
Purpose of the Study:
- To investigate the role of miR-382-5p in pulmonary inflammation induced by fine particulate matter (PM2.5) and diesel exhaust particles (DEPs).
- To elucidate the underlying molecular mechanisms involving the miR-382-5p/CXCL12/MMP9 pathway in response to PM exposure.
Main Methods:
- In vitro and in vivo experiments using human bronchial epithelial (HBE) cells and a murine model.
- Analysis of miR-382-5p and CXCL12 expression levels following PM2.5 and DEP exposure.
- Functional assays including gene silencing, overexpression, and antagonism of CXCL12.
Main Results:
- miR-382-5p exhibited an anti-inflammatory role, with its expression downregulated by PM2.5 and DEPs.
- PM exposure increased CXCL12 and MMP9 expression via miR-382-5p inhibition, promoting inflammation.
- Overexpression of miR-382-5p and CXCL12 antagonism mitigated PM-induced inflammation, apoptosis, and cell cycle arrest.
Conclusions:
- The miR-382-5p/CXCL12/MMP9 pathway is a critical mechanism mediating pulmonary inflammatory responses to PM2.5 and DEP exposure.
- Targeting this pathway holds potential for therapeutic interventions against PM-induced lung injury.
