RT Journal Article
SR Electronic
T1 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
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P3900
VO 44
IS Suppl 58
A1 Kazuhiro Yamada
A1 Kazuhisa Asai
A1 Yuko Ohara
A1 Yukari Sugiyama
A1 Atsuko Shirai
A1 Kanako Sato
A1 Norio Yamamoto
A1 Gakuya Tamagaki
A1 Tetsuya Watanabe
A1 Kazuhisa Konishi
A1 Yoshihiro Tochino
A1 Masato Uji
A1 Hiroshi Kanazawa
A1 Kazuto Hirata
YR 2014
UL http://erj.ersjournals.com/content/44/Suppl_58/P3900.abstract
AB IntroductionCigarette 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.AimThe aim of this study was to clarify the effect of cigarette smoke on PI3Ks and PTEN expression in human airway epithelial cells.MethodsBronchoscopic 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.ResultsThe 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).ConclusionCigarette smoke altered PI3KCD/PTEN balance in human airway epithelial cells.