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Obstructive Lung Diseases: COPD: Etiology |

The Effects of Caveolin-1 on Cigarette Smoke Extract-Induced MUC5AC Secretion in Human Airway Epithelial Cells FREE TO VIEW

Qiao Yu, PhD; Qiong Chen
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Xiangya Hospital of Central South Universtity, Changsha, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A357. doi:10.1016/j.chest.2016.02.372
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SESSION TITLE: COPD: Etiology

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: We aimed to determine whether caveolin-1 modulates MUC5AC hypersecretion induced by cigarette smoke.

METHODS: We employed gain- and loss-function approaches to assess the effects of caveolin-1 on the MUC5AC secretion stimulated by CSE and the underlying mechanism.

RESULTS: Our results revealed that cigarette smoke extract (CSE) significantly increased MUC5AC production, as well as the levels of phosphorylated EGFR (p-EGFR) and phosphorylated Akt (p-Akt) in human bronchial epithelial cells (16HBE cells), as shown by ELISA, RT-PCR and western blot analysis. These effects were prevented by treatment with EGFR inhibitor (AG1478) and phosphatidylinostol-3-kinase (PI3K) inhibitor (LY294002). We also found that the overexpression of caveolin-1 enhanced the expression of MUC5AC, p-EGFR and p-Akt induced by CSE. Conversely, the downregulation of caveolin-1 by siRNA against caveolin-1 inhibited the expression of MUC5AC, p-EGFR and p-Akt.

CONCLUSIONS: Taken together, our data suggest that caveolin-1 enhances CSE-induced MUC5AC hypersecretion through the EGFR/PI3K/Akt signaling pathway.

CLINICAL IMPLICATIONS: We demonstrated for the first time that caveolin-1 plays a helpful role in CS-induced MUC5AC secretion in 16HBE cells. We also evidenced that the effects of caveolin-1 involves EGFR/PI3K/Akt signal pathway. We speculate that down-regulation of caveolin-1 will protect against mucus hyper-secretion induced by CSE. Caveolin-1 may be a potential target for treatment of CS-induced mucus hyper-secretion in COPD.

DISCLOSURE: The following authors have nothing to disclose: Qiao Yu, Qiong Chen

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