Related Experiment Video
Updated: Aug 30, 2025
Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
Published on: September 20, 2024
MiR-217-5p inhibits smog (PM2.5)-induced inflammation and oxidative stress response of mouse lung tissues and
Jianli Xie1, Shaohua Li2, Xiaoning Ma3
1Department of Rheumatic Immunology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Objective:
To explore the roles of macrophages' miR-217-5p in the process of PM2.5 induced acute lung injury.
Methods:
GEO database and KEGG pathway enrichment analysis as well as GSEA were used to predicted the miRNA and associated target signals. And then mice and RAW246.7 macrophages treated with PM2.5 to imitate PM2.5 induced acute lung injury environment and then transfected with miR-217-5p NC or miR-217-5p mimic. The levels of inflammatory factors TNF-α and anti-inflammatory factor IL-10 of mice serum were tested by ELISA. And the pathological changes and ROS level of mouse lung tissues were stained by HE and DHE staining. The proteins expression of phosphorylated-STAT1, total-STAT1, TNF-α, IFN-γ as well as p47, gp91, NOX4 in mice or RAW264.7 cells were tested by western blot or immunofluorescence of RAW264.7 cell slides.
Results:
The results of bioinformatics analysis indicated the miR-217 as well as STAT1 were involved PM2.5 associated lung injury. After exposure to PM2.5, the decreased levels of serum TNF-α but not IL-10, consistent with reduced macrophages' accumulation as well as decreased ROS levels in lung tissues in miR-217-5p mimic group vs miR-217-5p NC group mice, and moreover, the protein expression levels of phosphorylated--STAT1, total-STAT1, TNF-α, IFN-γ, p47, gp91 and NOX4 in mouse lung tissues and RTAW246.7 macrophages cells were all significantly reduced with miR-217-5p mimic administration. The above phenomena were reversed by specific STAT1-inhibitor HY-N8107.
Conclusions:
miR-217-5p suppressed the activated STAT1-signal induced inflammation and oxidative stress trigged by PM2.5 in macrophages and resulted in the decreased lung injure caused by PM2.5.
Insights
MicroRNA-217-5p mitigates PM2.5-induced lung injury by suppressing STAT1-mediated inflammation and oxidative stress in macrophages, offering a potential therapeutic target.
Area of Science:
- * Molecular biology
- * Immunology
- * Environmental health
Background:
- * Particulate matter 2.5 (PM2.5) exposure is a significant risk factor for acute lung injury.
- * Macrophages play a crucial role in the inflammatory response to PM2.5.
- * MicroRNAs (miRNAs) are implicated in regulating cellular responses to environmental insults.
Purpose of the Study:
- * To investigate the role of miR-217-5p in macrophages during PM2.5-induced acute lung injury.
- * To elucidate the molecular mechanisms by which miR-217-5p affects inflammation and oxidative stress.
- * To assess the therapeutic potential of miR-217-5p in mitigating PM2.5 lung injury.
Main Methods:
- * Bioinformatics analysis (GEO, KEGG, GSEA) to identify relevant miRNA and target signals.
- * In vitro and in vivo models using RAW264.7 macrophages and mice exposed to PM2.5.
- * Transfection with miR-217-5p mimic or negative control (NC).
- * Measurement of inflammatory cytokines (TNF-α, IL-10), oxidative stress markers (ROS), and protein expression (STAT1, IFN-γ, NOX4 components) via ELISA, HE/DHE staining, Western blot, and immunofluorescence.
Main Results:
- * Bioinformatics analysis identified miR-217 and STAT1 involvement in PM2.5 lung injury.
- * PM2.5 exposure led to increased inflammation and oxidative stress, which were reduced by miR-217-5p mimic administration.
- * miR-217-5p mimic significantly decreased the expression of phosphorylated-STAT1, TNF-α, IFN-γ, and key proteins in the NADPH oxidase complex (p47, gp91, NOX4).
- * STAT1 inhibition reversed the protective effects of miR-217-5p mimic.
Conclusions:
- * miR-217-5p acts as a suppressor of STAT1 signaling in macrophages.
- * This suppression mitigates PM2.5-induced inflammation and oxidative stress.
- * miR-217-5p demonstrates potential as a therapeutic agent against PM2.5-induced lung injury.
More Related Videos
09:25Methods to Evaluate Cytotoxicity and Immunosuppression of Combustible Tobacco Product Preparations
Published on: January 10, 2015
08:15Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
Published on: June 6, 2025