Altered phenotype of COPD primary fibroblasts from airway and alveolar tissues: proliferation and apoptosis

Abstract

The pathological features of COPD are small airway remodeling and emphysema; the former is caused by excessive extracellular matrix (ECM) deposition, and the latter is owe to insufficient ECM repair. It is adjacent tissue in the same lung but present opposite ECM turnover. Fibroblasts are important cells to generate ECM and regulate its turnover. Previous research demonstrated that cells with different conditions might have different cell proliferation and apoptosis, which may be the source of COPD mechanism. It is unclear whether there are differences between fibroblasts from COPD airway and alveolar tissues. To investigate the proliferation and apoptosis of fibroblasts from COPD airway and alveolar tissues, as well as the response of two different regions of fibroblasts to TGF-β1. The proliferation and apoptosis of fibroblasts from COPD airway and alveolar tissues, with or without TGF-β1 stimulation, were detected by Alamar Blue and flow cytometry assay respectively. In our research, the proliferative ability of fibroblasts from COPD airway tissues was higher than that from COPD alveolar tissues, whereas the apoptosis of fibroblasts showed a low level in COPD airway compared with that in COPD alveoli. Moreover, the proliferative ability of fibroblasts from COPD airway tissues was elevated after TGF-β1 stimulation, whereas the COPD alveolar fibroblasts were not. The apoptosis of COPD alveolar fibroblasts was significantly increased after TGF-β1 stimulation compared with that of COPD airway fibroblasts. Therefore, there might be significantly differences between fibroblasts from COPD airway and alveolar tissues in terms of the cell proliferation and apoptosis.