PM2.5 induces autophagy via inhibition of the PI3K/Akt/mTOR kinasesignaling pathway in human bronchial epithelial cells
作者单位：广东医学院临床医学研究中心
会议名称：《中国生物化学与分子生物学会第十一次会员代表大会暨2014年全国学术会议》
会议日期：2014年
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
关 键 词：PM2.5 Autophagy Beas 2B Asthma PI3K/Akt/mTOR
摘 要：Particulate matter(PM2.5) is an important risk factor for asthma. Recent study showed autophagy is associated with asthma pathogenesis. However, the exact mechanisms underlyingPM2.5-induced autophagy in asthma are poorly understood. In this work, we evaluated the PM2.5-induced autophagy in Beas-2B cells and analyzed the possible molecular mechanism. Using electron microscopy, immunofluorescence staining, and immunoblot studies, we confirmed that PM2.5 caused autophagy in Beas-2B cells;PM2.5 inhibited phosphatidyl inositol 3-kinase(PI3K)/Akt/ mTOR pathway in Beas-2B cells. LY294002, aPI3 K inhibitor, alone reduced the accumulation of LC3 II and attenuated the effect ofPM2.5. p-p38, p-ERK and p-JNK were dephosphorylated after exposure to PM2.5. We also observed the role of p53, ROS scavenger(tetramethylthiourea) and autophagy inhibitor(3-methyladenine) on PM2.5-induced autophagy in Beas-2B cells. Our data suggest the possibility that PI3K/Akt/mTOR signaling pathway may be key contributor to the PM2.5-induced autophagy in Beas-2B cells. Our findings provide a insight into for possible future clinical applications targeting these signaling pathways in the management of PM2.5-induced lung disease.