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Effect of Urban Particulate Matter on Vocal Fold Fibrosis through the MAPK/NF-κB Signaling Pathway
Ho-Ryun Won1, Seung-Nam Jung1, Min-Kyung Yeo2
1Department of Otolaryngology-Head and Neck Surgery, College of Medicine, Chungnam National University, Daejeon 35015, Korea.
Abstract:
Particulate matter (PM) is an environmental exposure factor that adversely affects human health. PM is a risk factor for various diseases. However, the mechanism by which PM affects the vocal folds (VF) has not yet been evaluated. Thus, we investigated the cytotoxic effects of PM on human vocal fold fibroblasts (hVFF) and the underlying signaling pathways. hVFF were isolated from human VF. The effect of PM on hVFF, and the underlying mechanism, were analyzed using Western blot, quantitative real-time polymerase chain reaction, and flow cytometry. In addition, a histological evaluation was performed in animal experiments. Cell proliferation decreased after the PM treatment. PM increased the expression of interleukin (IL)-6 and IL-1β. The generation of reactive oxygen species (ROS) in PM-treated hVFF and subsequent activation of the mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways were confirmed. Furthermore, PM increased the expression of fibrosis-related markers and induced the accumulation of collagen in the extracellular matrix. As a result, PM exposure significantly enhances the inflammatory response on VF through the ROS-mediated activation of the MAPK and NF-κB signaling pathways. In addition, PM promotes differentiation into myofibroblasts and induces fibrosis. These results suggest that PM triggers an inflammatory reaction through ROS production and causes VF fibrosis.
Insights
Particulate matter (PM) exposure causes vocal fold inflammation and fibrosis by increasing oxidative stress and activating key signaling pathways. This study reveals PM
Area of Science:
- Environmental health
- Cell biology
- Fibrosis research
Background:
- Particulate matter (PM) is a known environmental health risk.
- PM's impact on vocal fold (VF) mechanisms is largely unknown.
- Understanding PM's cellular effects on VF is crucial for public health.
Purpose of the Study:
- Investigate PM's cytotoxic effects on human vocal fold fibroblasts (hVFF).
- Elucidate the signaling pathways involved in PM-induced VF damage.
- Assess PM's role in VF inflammation and fibrosis.
Main Methods:
- Primary human vocal fold fibroblasts (hVFF) were cultured.
- PM exposure effects analyzed via Western blot, qPCR, and flow cytometry.
- Histological analysis performed in animal models.
Main Results:
- PM exposure reduced hVFF proliferation and increased inflammatory markers (IL-6, IL-1β).
- PM induced reactive oxygen species (ROS) generation, activating MAPK and NF-κB pathways.
- PM promoted myofibroblast differentiation, collagen accumulation, and VF fibrosis.
Conclusions:
- PM exposure triggers vocal fold inflammation via ROS-mediated MAPK and NF-κB activation.
- PM contributes to vocal fold fibrosis by promoting myofibroblast differentiation.
- PM poses a significant risk for vocal fold damage and dysfunction.
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