Role of notch signaling pathway in Muc5ac secretion induced by atmospheric PM2.5 in rats
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Updated: Oct 10, 2025
Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins
Published on: June 14, 2016
Ying Liu1, Liting Zhou2, Hanlin Wu3
1Department of Respiratory Medicine, the First Hospital of Jilin University, Jilin University, Changchun, China.
Background:
The secretion of Muc5ac is closely related to the pathogenesis, treatment and prognosis of bronchial asthma. Atmospheric PM2.5 entered the airway can irritate and corrode the bronchial wall, affecting the expression and secretion of Muc5ac. However, the underlying mechanism is not clear. In this study, we investigated the role of the Notch signaling pathway in mucin section induced by atmospheric PM2.5 in rats.
Methods:
Fifty rats were divided randomly into five groups: the control received physiological saline; the health, health Notch signaling pathway inhibition and asthma, asthma Notch signaling pathway inhibition groups received 7.5 mg/kg PM2.5. PM2.5 or saline was instilled into the trachea at 2-day intervals for two doses. IL-1β, TNF-α and Muc5ac levels were detected by ELISA. The mRNA expression levels of Notch signaling pathway genes were detected by real time PCR. The levels of Notch signaling pathway protein were detected by western blot.
Results:
The levels of Muc5ac in the lungs and TNF-α in serum of asthmatic rats exposed to PM2.5 was the highest, and when Notch signaling pathway was inhibited, the levels of Muc5ac in the lungs and tracheas and TNF-α in serum of asthmatic rats exposed to PM2.5 was significantly decreased. Hes1 mRNA expression level in trachea was the lowest in the asthma inhibition group; and inhibiting the Notch signaling pathway could decrease the mRNA and protein levels of Hes1 in rats' lung. The mRNA relative levels of Notch3 and Notch4 in rats' trachea, the protein levels of Notch3 in rats' lung, and the mRNA relative levels of Jagged1 and Jaggeed2 in rats' lung were more consist with the changes of Muc5ac, TNF-α and Hes1.
Conclusion:
Notch signaling pathway played an important role in Muc5ac secretion induced by atmospheric PM2.5 of the asthmatic rats' airways. Jagged1 and Jagged2 interacting with Notch3 and Notch4 regulated the expression of Hes1, further regulated TNF-α in the process of PM2.5 inducing the secretion of Muc5ac.
Insights
Atmospheric particulate matter (PM2.5) increases MUC5AC secretion in asthma via the Notch pathway. Inhibiting this pathway reduces MUC5AC and TNF-α levels, suggesting a therapeutic target for PM2.5-induced airway inflammation.
Area of Science:
- Environmental Health
- Respiratory Medicine
- Molecular Biology
Background:
- Mucin MUC5AC secretion is critical in bronchial asthma pathogenesis.
- Atmospheric PM2.5 irritates airways, affecting MUC5AC but the mechanism is unclear.
Purpose of the Study:
- Investigate the Notch signaling pathway's role in PM2.5-induced mucin secretion in rats.
- Elucidate the molecular mechanisms linking PM2.5 exposure, airway inflammation, and MUC5AC production.
Main Methods:
- Rats were exposed to PM2.5 or saline, with and without Notch pathway inhibition.
- Measured MUC5AC, IL-1β, and TNF-α levels via ELISA.
- Assessed Notch pathway gene and protein expression using real-time PCR and Western blot.
Main Results:
- PM2.5 exposure elevated MUC5AC and TNF-α in asthmatic rats.
- Notch pathway inhibition significantly reduced MUC5AC and TNF-α levels.
- Jagged1/2, Notch3/4, and Hes1 expression correlated with MUC5AC and TNF-α changes.
Conclusions:
- The Notch signaling pathway is crucial for PM2.5-induced MUC5AC secretion in asthmatic airways.
- Jagged1/2-Notch3/4 interactions regulate Hes1, influencing TNF-α and MUC5AC production during PM2.5 exposure.
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