Dataset Information

Effect of Urban Particulate Matter on Vocal Fold Fibrosis through the MAPK/NF-?B Signaling Pathway.

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-1?. The generation of reactive oxygen species (ROS) in PM-treated hVFF and subsequent activation of the mitogen-activated protein kinase (MAPK) and nuclear factor-?B (NF-?B) 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-?B 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.

SUBMITTER: Won HR

PROVIDER: S-EPMC7555340 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Effect of Urban Particulate Matter on Vocal Fold Fibrosis through the MAPK/NF-κB Signaling Pathway.

Won Ho-Ryun HR Jung Seung-Nam SN Yeo Min-Kyung MK Yi Shinae S Liu Lihua L Lim Mi Ae MA Oh Chan C Kang Yea Eun YE Chang Jae Won JW Rha Ki Sang KS Koo Bon Seok BS

International journal of molecular sciences 20200910 18

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 ...[more]

PMID: 32927894

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Project description:Fine particulate matter (PM2.5) is a type of small particle that is <2.5 µm in diameter that may cause airway inflammation. Thus, the present study aimed to explore the effects of PM2.5 on endoplasmic reticulum (ER) stress and airway inflammation in human airway epithelial cells. For this purpose, HBE135‑E6E7 airway epithelial cells were cultured and exposed to specific concentrations of PM2.5 for various periods of time, and cell viability was determined using a Cell Counting Kit‑8 assay. The results of the present study demonstrated that exposure to PM2.5 increased the mRNA and protein expression levels of interleukin (IL)‑6, tumor necrosis factor (TNF)‑α and mucin 5AC (MUC5AC). Moreover, the expression levels of ER stress‑related proteins, such as glucose‑regulated protein 78, CCAAT‑enhancer binding protein homologous protein, activating transcription factor 6, protein kinase R‑like ER kinase (PERK), phosphorylated (p‑)PERK, inositol‑requiring enzyme 1α (IRE1α) and p‑IRE1α, and nucleotide‑binding oligomerization domain 1 (NOD1) expression levels were increased following exposure to PM2.5. Transfection with IRE1α small interfering RNA (siRNA) led to the increased production of IL‑6, TNF‑α and MUC5AC. Moreover, the expression of NOD1 and the translocation of NF‑κB p65 were inhibited following transfection with IRE1α siRNA. In addition, the results of the present study demonstrated that transfection with NOD1 siRNA decreased the production of IL‑6, TNF‑α and MUC5AC, and decreased the translocation of NF‑κB p65. The expression levels of IL‑6, TNF‑α and MUC5AC were increased in the HBE135‑E6E7 cells following treatment with C12‑iE‑DAP, a NOD1 agonist. Moreover, treatment with C12‑iE‑DAP led to the activation of NF‑κB p65. Collectively, the results of the present study suggest that PM2.5 promotes airway inflammation and mucin production by activating ER stress in HBE135‑E6E7 airway epithelial cells, and that the IRE1α/NOD1/NF‑κB pathway may be involved in this process.

Dataset Information

Effect of Urban Particulate Matter on Vocal Fold Fibrosis through the MAPK/NF-?B Signaling Pathway.

Publications

Effect of Urban Particulate Matter on Vocal Fold Fibrosis through the MAPK/NF-κB Signaling Pathway.

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