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Effects of PM2.5 on mucus hypersecretion in airway through miR-133b-5p/EGFR/Claudin1/MUC5AC axis
Lerong Chen1, Liangliang Wu1, Xiaopeng Cheng1
1Department of Respiratory, Jiangxi Provincial Chest Hospital, Nanchang 330006, Jiangxi, China.
Objective:
To investigate the role of the EGFR/MAPK signaling pathway in PM2.5 in promoting the MUC5AC hypersecretion in airway and exacerbating airway inflammation.
Methods:
By establishing rat model exposed to PM2.5, overexpressing miR-133b-5p and Claudin1, the content of IL-1 and TNF-α in serum were detected by ELISA, the pathology of lung tissue was observed by HE staining, p-EGFR, Claudin1, MUC5AC, p-ERK1/2, p-JNK, p-p38 in rats lung tissue were detected by immunohistochemical and WB, the expression level of miR-133b-5p in rats lung tissue were detected by qPCR.
Results:
After the rats were exposed to PM2.5, the content of inflammatory factors in serum increased, the inflammatory damage of lung tissues occurred, the expression of miR-133b-5p was down-regulated, and the expression of MUC5AC protein was increased. The ELISA test results showed that the expression of IL-1 and TNF-α in the model group was significantly higher than that in the control group, and the model +AG1478 treatment group was down-regulated compared with the model group, and the +miR-133b-5p agomir treatment group was significantly lower than that in the control group, the model group and the model +Claudin1 overexpression blank load group, and the model +Claudin1 overexpression group was down-regulated compared with the model group and the model +Claudin1 overexpression blank load group. The protein detection results showed that the expression of p-EGFR, MUC5AC, p-ERK1/2, p-JNK and p-p38 proteins was increased and the expression of Claudin1 protein was decreased in the model group compared with the control group. In the model + AG1478 treatment group, model + miR-133b-5p agomir treatment group and model + Claudin1 overexpression group, compared with the model group, p-EGFR, MUC5AC, p-ERK1/2, p-JNK, p-p38 protein expression was down-regulated, and Claudin1 protein expression was up-regulated.
Conclusions:
PM2.5 inhibited the expression of miR-133b-5p to activate the EGFR/MAPK signal pathway, induce the hypersecretion of MUC5AC, thus aggravating PM2.5-related airway inflammation in rats.
Insights
Particulate matter (PM2.5) exposure downregulates miR-133b-5p, activating the EGFR/MAPK pathway. This leads to MUC5AC hypersecretion and exacerbates airway inflammation in rats.
Area of Science:
- Environmental Health
- Molecular Biology
- Respiratory Medicine
Background:
- Particulate matter (PM2.5) is a major air pollutant linked to respiratory diseases.
- The EGFR/MAPK signaling pathway plays a critical role in airway inflammation and mucus production.
- MicroRNAs (miRNAs) are emerging as key regulators in various biological processes, including inflammation.
Purpose of the Study:
- To elucidate the role of the EGFR/MAPK signaling pathway in PM2.5-induced MUC5AC hypersecretion and airway inflammation.
- To investigate the involvement of miR-133b-5p in this process.
Main Methods:
- A rat model was established by exposing rats to PM2.5.
- Interventions included overexpression of miR-133b-5p and Claudin1.
- Key markers such as IL-1, TNF-α, p-EGFR, MUC5AC, p-ERK1/2, p-JNK, p-p38, and miR-133b-5p were measured using ELISA, HE staining, immunohistochemistry, Western blot, and qPCR.
Main Results:
- PM2.5 exposure increased serum inflammatory factors (IL-1, TNF-α) and lung tissue damage.
- miR-133b-5p expression was downregulated, while MUC5AC protein expression was increased in PM2.5-exposed rats.
- Activation of the EGFR/MAPK pathway (increased p-EGFR, p-ERK1/2, p-JNK, p-p38) and decreased Claudin1 expression were observed.
Conclusions:
- PM2.5 inhibits miR-133b-5p expression, leading to the activation of the EGFR/MAPK signaling pathway.
- This activation induces MUC5AC hypersecretion, consequently aggravating PM2.5-related airway inflammation in rats.
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