title: Dynamic investigation of alveolar type II cell function in a long-term survival model of rat lung ischemia-reperfusion injury.
abstract: BACKGROUND
  Alveolar type II (ATII) cells are capable of repairing the alveolar epithelium injury induced by lung ischemia-reperfusion injury (LIRI). In the present study, we aim to dynamically investigate the morphological and functional alternations of ATII cells using a long-term survival model of rat LIRI.
  
  
  METHODS
  Male Sprague-Dawley rats were randomized into sham and ischemia-reperfusion (IR) groups. Animals of IR group underwent warm ischemia for 60 minutes by left pulmonary hilum occlusion. Injury was assessed by histological examination and myeloperoxidase activity assay. The proliferation profile of ATII cells was evaluated by immunofluorescence double staining. Surfactant protein-C (SP-C) and caspase-3 expression were determined by reverse transcription polymerase chain reaction. Ultrastructure and stereological analysis were used to quantify the alterations of nuclei and lamellar bodies (LBs) of ATII cells.
  
  
  RESULTS
  As compared with the sham group, SP-C expression in the IR group significantly decreased at the early phase of LIRI and returned to normal in 7 days after reperfusion. SP-C/PCNA double positive cell number significantly increased at 1d, peaked at 3d and decreased to normal until 7 days after reperfusion. Ultrastructure and stereological analysis of ATII cells also showed that LBs were remarkably impaired at the early phase of LIRI and recovered up to 7 days after reperfusion.
  
  
  CONCLUSIONS
  This model is simple, stable and reproducible. ATII cells demonstrated a self-repair capacity in a slow manner following the early phase of LIRI. Enhancing self-repair capacity of ATII cells may be a potential way of alleviating or curing LIRI.
authors.affiliation: Department of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital of Jiangsu Province, Cancer Institution of Jiangsu Province, Nanjing, P. R. China.
authors.forename: Dongjie
authors.initials: D
authors.lastname: Feng
authors.forename: Shuai
authors.initials: S
authors.lastname: Zhang
authors.forename: Zhendong
authors.initials: Z
authors.lastname: Hu
authors.forename: Frank
authors.initials: F
authors.lastname: Fan
authors.forename: Feng
authors.initials: F
authors.lastname: Jiang
authors.forename: Rong
authors.initials: R
authors.lastname: Yin
authors.forename: Lin
authors.initials: L
authors.lastname: Xu
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000096:biosynthesis; D004195:Disease Models, Animal; D008168:Lung / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008856:Microscopy, Fluorescence; D010455:Peptides / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000166:cytology* / Q000473:pathology / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology
chemical_list: D010455:Peptides; D012333:RNA, Messenger; C077063:Sftpc protein, rat; D053148:Caspase 3