title: [Silencing of Pin1 suppresses hyperoxia-induced apoptosis of A549 cells].
abstract: OBJECTIVE
  To explore the effect of silence of Pin1 expression on hyperoxia-induced apoptosis in alveolar epithelial cells A549.
  
  
  METHODS
  A549 cells were divided into four groups: control, hyperoxia, negative lentivirus and Pin1-shRNA hyperoxia. The hyperoxia group was exposed to a mixture of 95%O2 and 5%CO2 for 10 minutes. Then cells were cultured in a closed environment. After 24 hours, the changes of morphology were observed under an inverted microscope. Cell apoptosis was detected by flow cytometry (FCM). The expression of X-linked inhibitor of apoptosis protein (XIAP) and Caspase-9 were detected by immunohistochemistry. The production of reactive oxygen species (ROS) and cellular mitochondria membrane potential (△Ψm) were determined by fluorescence microscopy.
  
  
  RESULTS
  Under the inverted microscope, the A549 cells grew slowly and the changes in morphology of the cells were most obvious in the hyperoxia and negative lentivirus groups. The changes in morphology of A549 cells were obviously improved in the Pin1-shRNA hyperoxia group. The FCM results showed that the apoptosis rate of A549 cells increased, Caspase-9 expression increased, XIAP expression decreased, mitochondrial ROS production increased and mitochondrial membrane potential decreased in the hyperoxia and negative lentivirus groups compared with the control group (P<0.05). Compared with the hyperoxia and negative lentivirus groups, the apoptosis rate of A549 cells decreased, Caspase-9 expression decreased, XIAP expression increased, mitochondrial ROS production decreased and mitochondrial membrane potential increased in the Pin1-shRNA hyperoxia group (P<0.05), although the levels of the indexes did not reach to those of the control group.
  
  
  CONCLUSIONS
  Silencing of Pin1 could suppress hyperoxia-induced apoptosis of A549 cells.
authors.affiliation: Department of Neonatology, Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan 646000, China. dongwenbin2000@163.com.
authors.forename: Shuai
authors.initials: S
authors.lastname: Zhao
authors.forename: Wen-Bin
authors.initials: WB
authors.lastname: Dong
authors.forename: Chan
authors.initials: C
authors.lastname: Zhang
authors.forename: Qing-Ping
authors.initials: QP
authors.lastname: Li
authors.forename: Lan
authors.initials: L
authors.lastname: Kang
authors.forename: Xiao-Ping
authors.initials: XP
authors.lastname: Lei
authors.forename: Xue-Song
authors.initials: XS
authors.lastname: Zhai
mesh_terms: D017209:Apoptosis; D053453:Caspase 9 / Q000235:genetics; D006801:Humans; D018496:Hyperoxia / Q000473:pathology*; D053078:Membrane Potential, Mitochondrial; D000072340:NIMA-Interacting Peptidylprolyl Isomerase; D019696:Peptidylprolyl Isomerase / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D051636:X-Linked Inhibitor of Apoptosis Protein / Q000235:genetics
chemical_list: D000072340:NIMA-Interacting Peptidylprolyl Isomerase; D017382:Reactive Oxygen Species; D051636:X-Linked Inhibitor of Apoptosis Protein; C496866:XIAP protein, human; D053453:Caspase 9; C000606846:PIN1 protein, human; D019696:Peptidylprolyl Isomerase