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PM2.5 deregulated microRNA and inflammatory microenvironment in lung injury
Guangyan Liu1, Yunxia Li2, Jiaming Zhou3
1Department of Pathogen Biology, Shenyang Medical College, No. 146, Huanghe North Street, Shenyang, People's Republic of China.
Abstract:
PM2.5 negatively affects human health, particularly lung injury. However, the role of PM2.5-regulated miRNAs in lung injury remains unknown. MiRNA array results showed mmu-miR-467c-5p regulated Prdx6 expression to adapt to lung injury condition, and deregulated miRNAs regulated macrophages to build a localized inflammatory microenvironment. In addition, miRNAs were transferred into adjacent alveolar epithelial cells, regulating the expressions of cell injury signaling pathway-targeted genes, and accelerating local lung tissue injury. NO and RAGE were increased in the coculture supernatant, and SPD was decreased. PM2.5 exposure induced local lung injury, promoted inflammation in local lung tissues, increased capillary permeability in the lung tissue, and rearranged the local lung tissue structure. We also confirmed in AECOPD patients TNF-α and IL-1β levels are obviously higher than healthy person. These findings provide new mechanistic insights regarding PM2.5 and targeted miRNAs in the inflammatory microenvironment, which increases our knowledge of PM2.5-lung injury interactions.
Insights
Fine particulate matter (PM2.5) causes lung injury by altering microRNAs (miRNAs) that regulate inflammation and cell damage. These findings reveal new mechanisms in PM2.5-induced lung disease.
Area of Science:
- Environmental Health
- Molecular Biology
- Pulmonology
Background:
- Particulate matter (PM2.5) exposure is a significant risk factor for adverse respiratory health outcomes.
- The specific molecular mechanisms by which PM2.5 induces lung injury, particularly involving microRNAs (miRNAs), are not fully understood.
Purpose of the Study:
- To investigate the role of PM2.5-regulated miRNAs in the pathogenesis of lung injury.
- To elucidate the cellular and molecular pathways involved in PM2.5-induced lung inflammation and tissue damage.
Main Methods:
- MiRNA array analysis was performed to identify differentially expressed miRNAs in response to PM2.5 exposure.
- Co-culture systems were used to study miRNA transfer between cells and their effects on signaling pathways.
- Biochemical assays measured inflammatory markers and cell injury indicators.
Main Results:
- PM2.5 exposure altered miRNA expression, notably mmu-miR-467c-5p, affecting Prdx6 expression and macrophage-driven inflammation.
- Transferred miRNAs modulated cell injury signaling pathways in adjacent alveolar epithelial cells.
- Increased levels of nitric oxide (NO) and receptor for advanced glycation end products (RAGE), with decreased surfactant protein D (SPD), were observed.
- PM2.5 exposure led to lung tissue damage, inflammation, increased capillary permeability, and structural alterations.
- Patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) showed elevated TNF-α and IL-1β levels.
Conclusions:
- PM2.5 induces lung injury through miRNA-mediated regulation of inflammatory microenvironments and cell signaling.
- MiRNA dysregulation contributes to PM2.5-induced lung tissue damage and inflammation.
- These findings enhance understanding of the complex interactions between PM2.5, miRNAs, and lung injury, with implications for AECOPD.
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