Abstract
The airway epithelium is a dynamic tissue that undergoes slow but constant renewal. Dysregulation of airway epithelial cell function related to cigarette smoke exposure plays an important role in the pathophysiology of COPD and is associated to tissue damage and disease severity. Oct-4 is the crucial POU domain transcription factor responsible for maintaining cellular self-renewal and regeneration, and CD146 is an adhesion molecule involved in outside-in signalling of inflammatory processes, remodeling and cell proliferation.
The aim of the present study was to investigate the mechanisms involved in airway epithelium maintenance and injury-induced regeneration and their correlation with Oct-4 and CD146 protein expression.
We studied the expression of Oct-4 and CD146 protein by western blot and flow cytometry in human bronchial epithelial cells (16HBE cells) exposed to 5% Cigarette Smoke Extract (CSE) for 120 hours.
We found that long term exposure to CSE significantly down-regulated Oct-4 protein expression in 16HBE cells, whereas CD146, that was not expressed in untreated cells, was significantly increased by CSE treatment. Accordingly, under oxidative stress conditions, an inverse correlation between Oct-4 and CD146 protein expression was observed.
Chronic exposure to cigarette smoke may be able to induce an altered epithelium homeostasis and regenerative capacity in bronchial epithelial cells. The Oct-4 gene activity down-regulation might lead to the imbalance between renewal, repair processes and pro-inflammatory and pro-oxidative mechanisms with a potential role in abnormal tissue remodeling and progression of COPD.
- © 2014 ERS
