title: Erythropoietin Receptor Activation Protects the Kidney From Ischemia/Reperfusion-Induced Apoptosis by Activating ERK/p53 Signal Pathway.
abstract: BACKGROUND
  Apoptosis plays an important role in renal ischemia/reperfusion (IR) injury. Evidence has shown that erythropoietin (EPO) has an antiapoptotic effect. Therefore, this study aimed to explore the effect and potential mechanism of EPO in renal IR injury.
  
  
  METHODS
  Kidney IR injury in rats was established by clamping the left renal artery for 30 minutes followed by 24 hours of reperfusion, along with contralateral nephrectomy. Renal function, renal histology, and expression of EPOR, p-EPOR, ERK, p-ERK, p-p53, p53, Bcl-2, Bcl-xl, Bad, and Bax were examined.
  
  
  RESULTS
  Pretreatment with EPO significantly reduced renal dysfunction, pathologic change, and expression of Bad and Bax. Furthermore, EPO treatment enhanced the expression of p-ERK, p-p53, Bcl-2, and Bcl-xl with no influence on the expression of EPOR, ERK, and p53.
  
  
  CONCLUSIONS
  These findings demonstrated that EPO pretreatment can attenuate renal IR injury by inhibiting apoptosis by promoting activation of the ERK/p53 signaling.
authors.affiliation: Department of Nephrology, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.
authors.forename: Y-R
authors.initials: YR
authors.lastname: Zou
authors.affiliation: Department of Nephrology, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of General Medicine, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.affiliation: Department of Nephrology, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China.
authors.forename: L
authors.initials: L
authors.lastname: Peng
authors.affiliation: Department of Nephrology, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China. Electronic address: guisenli@163.com.
authors.forename: G-S
authors.initials: GS
authors.lastname: Li
authors.affiliation: Department of Nephrology, Center of Electronic Science Technology and University of Electronic Science and Technology, Sichuan Academy of Sciences and Sichuan Provincial People's Hospital, Chengdu, People's Republic of China. Electronic address: scwangli62@163.com.
authors.forename: L
authors.initials: L
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D004921:Erythropoietin / Q000494:pharmacology*; D007511:Ischemia / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000293:injuries / Q000503:physiopathology; D020935:MAP Kinase Signaling System / Q000187:drug effects* / Q000502:physiology; D008297:Male; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017467:Receptors, Erythropoietin / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D051017:Apoptosis Regulatory Proteins; D020011:Protective Agents; D017467:Receptors, Erythropoietin; D016159:Tumor Suppressor Protein p53; D004921:Erythropoietin