title: Effects of ischemic preconditioning in the late phase on homing of endothelial progenitor cells in renal ischemia/reperfusion injury.
abstract: OBJECTIVE
  The aim of this study was to determine whether the mobilization and recruitment of endothelial progenitor cells (EPCs) contribute to the protection of kidneys from ischemia/reperfusion (I/R) injury after ischemic preconditioning (IPC) during the late phase.
  
  
  METHODS
  Seventy-five male Sprague-Dawley rats were divided into the following groups: sham-operated (group A; n = 25), ischemia/reperfusion hosts that underwent 45 minutes of left renal artery ischemia (group B; n = 25), and ischemic preconditioning-treated group (group C; n = 25). Group C underwent 3 cycles of 5 minutes of occlusion and 5 minutes of reperfusion followed by 24 hours of reperfusion before the following 45 minutes of occlusion. Serum samples were collected and renal tissues harvested for histological examination terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, immunohistochemical staining, and Western blot analysis to determine the expression levels of CD34, VEGFR-2 (Vascular Endothelial Growth Factor Receptor 2)/flk-1, vascular endothelial growth factor (VEGF), and stromal cell-derived factor-1α (SDF-1α).
  
  
  RESULTS
  Compared with group B, the levels of blood urea nitrogen (BUN), serum creatinine (Scr) and acute tubulointerstitial injury at 24 hours after operation were significantly reduced in group C. At 72 hours, tubular epithelial cell apoptosis was also decreased (17.6 ± 4.45 vs 63.8 ± 6.10; P < .01). CD34+ and flk-1+ cells that mostly accumulated in the medullopapillary parenchyma were significantly increased at 72 hours (P < .05). Expression levels of VEGF and SDF-1α were also significantly higher in group C (P < .05).
  
  
  CONCLUSIONS
  The present work suggested that IPC protected kidneys from IR injury in the later phase through enhanced mobilization and recruitment of EPCs. VEGF and SDF-1α may play important roles in this protective effect.
authors.affiliation: Department of Urology and Transplantation, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing, China.
authors.forename: C-J
authors.initials: CJ
authors.lastname: Bo
authors.forename: B
authors.initials: B
authors.lastname: Chen
authors.forename: R-P
authors.initials: RP
authors.lastname: Jia
authors.forename: J-G
authors.initials: JG
authors.lastname: Zhu
authors.forename: P
authors.initials: P
authors.lastname: Cao
authors.forename: H
authors.initials: H
authors.lastname: Liu
authors.forename: R
authors.initials: R
authors.lastname: Wu
authors.forename: Y-Z
authors.initials: YZ
authors.lastname: Ge
authors.forename: J-P
authors.initials: JP
authors.lastname: Wu
mesh_terms: D000818:Animals; D018952:Antigens, CD34 / Q000378:metabolism; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D001806:Blood Urea Nitrogen; D015153:Blotting, Western; D002465:Cell Movement; D054377:Chemokine CXCL12 / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000473:pathology*; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019194:Ischemic Preconditioning; D007668:Kidney / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D013234:Stem Cells / Q000473:pathology*; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism
chemical_list: D018952:Antigens, CD34; D015415:Biomarkers; D054377:Chemokine CXCL12; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D003404:Creatinine; D040301:Vascular Endothelial Growth Factor Receptor-2