【摘 要】
：
Ultrafine particles(UFPs)are capable of inducing pulmonary fibrosis(PF);however,the underlying molecular mechanisms have not been fully elucidated.Here,we reported an important role of autophagy in th
【机 构】
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Institute of Environmental Medicine,Zhejiang University School of Medicine,Hangzhou,310058;Program i
【出 处】
：
中国生物化学与分子生物学会2016年全国学术会议
论文部分内容阅读
Ultrafine particles(UFPs)are capable of inducing pulmonary fibrosis(PF);however,the underlying molecular mechanisms have not been fully elucidated.Here,we reported an important role of autophagy in the pathogenesis of UFP-induced PF.UFPs were endocytosed by Type Ⅱ alveolar epithelial cells(AECs)which stimulated PF development.UFPs increased autophagosome accumulation independent on mTOR activity and induced apoptosis.However,degradation of p62 was inhibited in UFPs-treated cells,indicating a blockage of autophagy flux.Furthermore,the inhibition of autophagic degradation contributed to a decreased lysosomal degradation capacity through impairment of lysosomal acidification instead of impaired autophagosome-lysosome fusion.Moreover,enhancement of autophagic degradation by rapamycin suppressed UFPs-induced apoptosis.These data suggest that a repressive effect of UFPs on lysosomal acidification contributes to the decreasedautophagic degradation in AECs,induction of apoptosis and initiation of PF.
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