The effect of smoking on phosphoinositide 3-kinase (PI3K) and phosphatase and tensin homolog deleted from chromosome 10 (PTEN) mRNA expression in human airway epithelial cells

Introduction Cigarette smoking, a major etiology of chronic obstructive pulmonary disease (COPD) , causes persistent airway inflammation.Phosphoinositide 3-kinases (PI3Ks) are family of enzyme involved in synthesis of phosphatidylinositol (3,4,5)-triphosphate (PtdIns(3,4,5)P3), which induce cellular functions such as cell growth, proliferation, differentiation and production of inflammatory mediator. In contrast, Phosphatase and Tensin Homolog Deleted from Chromosome 10 (PTEN) is known to be an endogenous inhibitor of PI3Ks. However, little is known regarding the effect of cigarette smoke on PI3Ks and PTEN expression. Aim The aim of this study was to clarify the effect of cigarette smoke on PI3Ks and PTEN expression in human airway epithelial cells. Methods Bronchoscopic brushing cells from twenty current smokers (15 COPD patients and 5 smoking non-COPD patients) and 7 healthy non-smoker were evaluated for PI3Kcatalytic delta polypeptide (PI3KCD) and PTEN mRNA expressions by RT-PCR. Results The ratio of PI3KCD to PTEN mRNA expression was significantly increased (p<0.05), while there were trends towards increased PI3KCD mRNA expression and decreased PTEN mRNA expression in smokers. Expression of PTEN mRNA in smokers was significantly correlated with Brinkman Index (r=-0.52, p<0.05). Conclusion Cigarette smoke altered PI3KCD/PTEN balance in human airway epithelial cells.