Cigarette smoke extract induces apoptosis of rat alveolar Type II cells via the PLTP/TGF-β1/Smad2 pathway

• Published in: International immunopharmacology 2015-09, Vol.28 (1), p.707-714
• Main Authors: Chen, Hong, Liao, Ke, Cui-Zhao, Lv, Qiang-Wen, Fu, Feng-Zeng, Xue, Ping-Wu, Feng, Liang-Guo, Shu, Juan-Chen, Ya
• Format: Article
• Language: English
• Subjects: Alveolar Type II cells; Animals; Apoptosis; Apoptosis - drug effects; Blotting, Western; Cell Line; Cell Proliferation - drug effects; Cigarette smoke extract; Dose-Response Relationship, Drug; Inhalation Exposure; Lung Injury - chemically induced; Lung Injury - immunology; Lung Injury - pathology; Male; Phospholipid transfer protein; Phospholipid Transfer Proteins - immunology; Phospholipid Transfer Proteins - metabolism; Pulmonary Alveoli - drug effects; Pulmonary Alveoli - immunology; Pulmonary Alveoli - pathology; Rats, Wistar; Real-Time Polymerase Chain Reaction; Signal Transduction; Smad2; Smad2 Protein - immunology; Smad2 Protein - metabolism; Smoke; Smoking - adverse effects; Tobacco Products - toxicity; Transforming Growth Factor beta1 - immunology; Transforming Growth Factor beta1 - metabolism; Transforming growth factor-β1
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2015.07.029

Apoptosis of alveolar epithelial cells has been implicated in the pathogenesis of acute lung injury. Phospholipid transfer protein (PLTP) may play a role in apoptosis. In the present study, the effect of the novel function of PLTP in cigarette smoke extract (CSE)-induced apoptosis of alveolar epithelial cells and the possible mechanism were examined. Male Wistar rats were exposed to air and cigarette smoke (n=10/exposure) for 6h/day on 3 consecutive days, then the lungs were sectioned and examined. To investigate effects on alveolar epithelial cells, rat alveolar epithelial cells (RLE-6TN) were treated with different concentrations of CSE for various times. siRNA for PLTP was transfected into cells and an inhibitor of the transforming growth factor-β1 (TGF-β1) type I receptor was administered prior to CSE exposure. Apoptosis was measured, and mRNA expression of PLTP and TGF-β1 and protein levels of PLTP, TGF-β1, p-Smad2 and cleaved caspase-3 were analyzed. The results showed that apoptosis, as well as expression of PLTP, TGF-β1, p-Smad2 and cleaved caspase-3 were all significantly increased after CSE stimulation (P