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Published on: June 14, 2016
PM2.5 Upregulates the Expression of MUC5AC via the EGFR-PI3K Pathway in Human Sinonasal Epithelial Cells
Jian Jiao1,2, Puqi Hu1,2,3, Ying Li1,2
1Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China.
Background:
Fine particulate matter (PM) (PM with an aerodynamic diameter <2.5 μm, PM2.5) exposure contributes to respiratory disease development and exacerbation.
Objective:
We sought to investigate the effect of PM2.5 exposure on mucociliary function in primary human nasal epithelial cells (HNECs) and the underlying mechanism.
Methods:
HNECs derived from control subjects and patients with chronic rhinosinusitis with nasal polyps were established as air-liquid interface cultures. Confluent cultures were exposed to 100 or 200 μg/mL PM2.5 for 24 h and assessed for expression of specific mucociliary-associated factors, the percentage of β-tubulin IV-positive and MUC5AC-positive cells, expression of epidermal growth factor receptor (EGFR) ligand and activation of phosphoinositide 3-kinase (PI3K)-AKT/ERK. In addition, cultures pretreated for 30 min with AG1478 (an EGFR inhibitor) or LY294002 (a PI3K inhibitor) following PM2.5 exposure were assessed for MUC5AC mRNA and protein expression.
Results:
PM2.5 exposure at 100 or 200 μg/mL for 24 h did not affect geminin coiled-coil domain containing, multiciliate differentiation and DNA synthesis associated cell cycle protein, FOXJ1, or DNAI2 mRNA expression or the percentage of β-tubulin IV-positive cells. However, 200 μg/mL PM2.5 exposure significantly increased mRNA expression of SAM-pointed domain-containing ETS transcription factor and MUC5AC and the percentage of MUC5AC-positive cells. PM2.5 also increased expression of EGFR ligands, including heparin-binding EGF-like growth factor and amphiregulin. Furthermore, PM2.5induced activation of PI3K, AKT, and ERK, and pretreatment of HNECs with AG1478 or LY294002 attenuated PM2.5-induced MUC5AC mRNA and protein expression.
Conclusions And Clinical Relevance:
This study demonstrates that short-term PM2.5 exposure increases MUC5AC expression in HNECs. Furthermore, this study shows that PM2.5-induced MUC5AC expression is likely mediated through the EGFR-PI3K pathway.
Insights
Short-term exposure to fine particulate matter (PM2.5) increases MUC5AC expression in human nasal cells. This effect is mediated by the epidermal growth factor receptor (EGFR) and phosphoinositide 3-kinase (PI3K) pathway.
Area of Science:
- Environmental Health
- Cell Biology
- Respiratory Medicine
Background:
- Fine particulate matter (PM2.5) is a significant contributor to respiratory disease.
- Understanding PM2.5's impact on airway epithelium is crucial for public health.
Purpose of the Study:
- To investigate the effect of PM2.5 on mucociliary function in primary human nasal epithelial cells (HNECs).
- To elucidate the underlying molecular mechanisms of PM2.5-induced changes in HNECs.
Main Methods:
- HNECs from healthy donors and chronic rhinosinusitis patients were cultured at an air-liquid interface.
- Cells were exposed to PM2.5 (100 or 200 μg/mL) for 24 hours.
- Key mucociliary factors, EGFR, PI3K/AKT/ERK pathways, and MUC5AC expression were assessed. Inhibitors of EGFR and PI3K were used to explore the mechanism.
Main Results:
- PM2.5 exposure (200 μg/mL) significantly increased MUC5AC mRNA and protein expression and the percentage of MUC5AC-positive cells.
- PM2.5 elevated the expression of EGFR ligands, heparin-binding EGF-like growth factor and amphiregulin.
- PM2.5 activated the PI3K/AKT and ERK signaling pathways, which was attenuated by EGFR and PI3K inhibitors.
Conclusions:
- Short-term PM2.5 exposure increases MUC5AC expression in HNECs.
- The EGFR-PI3K pathway is a key mediator of PM2.5-induced MUC5AC expression.
- Findings suggest a mechanism for PM2.5 in exacerbating respiratory conditions.
