title: Ischemic preconditioning increases endothelial progenitor cell number to attenuate partial nephrectomy-induced ischemia/reperfusion injury.
abstract: OBJECTIVE
  The objective of this study was to investigate the role of endothelial progenitor cells (EPCs) in the modulation of ischemia-reperfusion injury (IRI) in a partial nephrectomy (PN) rat model using early-phase ischemic preconditioning (IPC).
  
  
  METHODS
  Ninety male Sprague-Dawley rats were randomly divided into three groups following right-side nephrectomy: Sham-operated rats (surgery without vascular clamping); PN rats (renal blood vessels were clamped for 40 min and PN was performed); and IPC rats (pretreated with 15 min ischemia and 10 min reperfusion). At 1, 3, 6, 12, 24 h, and 3 days after reperfusion, the pool of circulating EPCs and kidneys were harvested. The extent of renal injury was assessed, along with EPC number, cell proliferation, angiogenesis, and vascular growth factor expression.
  
  
  RESULTS
  Pretreated rats exhibited significant improvements in renal function and morphology. EPC numbers in the kidneys were increased at 12 h following reperfusion in the IPC group as compared to the PN or Sham groups. Cell proliferation (including endothelial and tubular epithelial cells) and angiogenesis in peritubular capillaries were markedly increased in kidneys treated with IPC. In addition, vascular endothelial growth factor-A (VEGF-A) and stromal cell-derived factor-1α (SDF-1α) expression in the kidneys of pretreated rats was increased compared to rats subjected to PN.
  
  
  CONCLUSIONS
  OUR INVESTIGATION SUGGESTED THAT: (1) the early phase of IPC may attenuate renal IRI induced by PN; (2) EPCs play an important role in renal protection, involving promotion of cell proliferation and angiogenesis through release of several angiogenic factors.
authors: Department of Urology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
authors: Hao
authors: H
authors: Liu
authors: Ran
authors: R
authors: Wu
authors: Rui-Peng
authors: RP
authors: Jia
authors: Bing
authors: B
authors: Zhong
authors: Jia-Geng
authors: JG
authors: Zhu
authors: Peng
authors: P
authors: Yu
authors: Yan
authors: Y
authors: Zhao
authors: Yu-Zheng
authors: YZ
authors: Ge
authors: Jian-Ping
authors: JP
authors: Wu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D054377:Chemokine CXCL12 / Q000378:metabolism; D017931:DNA Primers / Q000235:genetics; D042783:Endothelial Cells / Q000502:physiology*; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006652:Histological Techniques; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D018919:Neovascularization, Physiologic / Q000502:physiology; D009392:Nephrectomy / Q000009:adverse effects*; D016133:Polymerase Chain Reaction; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000209:etiology* / Q000517:prevention & control*; D013234:Stem Cells / Q000502:physiology*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D054377:Chemokine CXCL12; D017931:DNA Primers; D042461:Vascular Endothelial Growth Factor A
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