title: G1 cell cycle arrest signaling in hepatic injury after intraperitoneal sepsis in rats.
abstract: OBJECTIVE
  Hepatocytes emerge from a quiescent state into a proliferative state to recover from septic injury. We hypothesize that hepatocyte cell cycle regulation after sepsis potentially contributes to the recovery of liver function.
  
  
  METHODS
  An animal model of sepsis was induced by cecal ligation and puncture (CLP) in rats. At serial time points after CLP, hepatocyte expression of p21, P53, cyclin D1, cyclin E, CDK2, CDK4 and PCNA was determined by immunoblot analysis, and the DNA content of isolated hepatocytes was analyzed using flow cytometry.
  
  
  RESULTS
  Sepsis-induced liver injury of rats was associated with G1 cell cycle arrest. Recovery of liver function was related to cell cycle progression 48 h after CLP. The upregulation of p53 and p21 correlated with G1 cell arrest 48 h after CLP. The upregulation of cyclin D1/CDK4 and cyclin E/CDK2 also correlated with the G1/S transition 48 h after CLP, resulting in PCNA expression.
  
  
  CONCLUSIONS
  The data suggests that G1 cell cycle arrest and p53, p21, CDKs, cyclins and PCNA expression may be involved in the injury/recovery of liver function after intraperitoneal sepsis.
authors.affiliation: Department of Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, 1 Shuaifuyuan, Dongcheng District, Beijing, 100730, China.
authors.forename: Quan-hui
authors.initials: QH
authors.lastname: Yang
authors.forename: Da-wei
authors.initials: DW
authors.lastname: Liu
authors.forename: Xiao-ting
authors.initials: XT
authors.lastname: Wang
authors.forename: Rong-li
authors.initials: RL
authors.lastname: Yang
authors.forename: Yan
authors.initials: Y
authors.lastname: Shi
authors.forename: Yun
authors.initials: Y
authors.lastname: Long
authors.forename: Hong-zhong
authors.initials: HZ
authors.lastname: Liu
authors.forename: Huai-wu
authors.initials: HW
authors.lastname: He
authors.forename: Xiang
authors.initials: X
authors.lastname: Zhou
authors.forename: Bo
authors.initials: B
authors.lastname: Tang
mesh_terms: D000818:Animals; D019938:Cyclin D1 / Q000378:metabolism; D019927:Cyclin E / Q000378:metabolism; D051357:Cyclin-Dependent Kinase 2 / Q000378:metabolism; D051358:Cyclin-Dependent Kinase 4 / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D016193:G1 Phase / Q000502:physiology*; D022781:Hepatocytes / Q000166:cytology / Q000502:physiology; D006801:Humans; D008099:Liver / Q000473:pathology* / Q000502:physiology*; D008297:Male; D051381:Rats; D018805:Sepsis / Q000473:pathology / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D019927:Cyclin E; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016159:Tumor Suppressor Protein p53; D019938:Cyclin D1; C495892:Cdk2 protein, rat; D051357:Cyclin-Dependent Kinase 2; D051358:Cyclin-Dependent Kinase 4