title: Postconditioning attenuates renal ischemia-reperfusion injury by mobilization of stem cells.
abstract: BACKGROUND
  We recently showed that reactive oxygen species (ROS) and mitochondrial DNA damage and deletions were attenuated by postconditioning (POC). It is not known, however, whether a population of progenitor cells is recruited by POC and is responsible for repair of renal tubular epithelial cells after ischemic injury.
  
  
  METHODS
  The model of renal POC was induced by 45 min clamping of the left renal artery and right nephrectomy followed by 7 min of short-time full reperfusion and 3 cycles of 30 s ischemia and 30 s reperfusion. The lymphocyte compartment of peripheral blood was evaluated by fluorescence-activated cell sorting (FACS) to determine expression of the bone marrow-derived progenitor cell markers CXC-chemokine receptor 4 (CXCR4), c-Kit, and CD34, at 12 h, 1 day and 3 days post-ischemia. Serum and kidney tissue were collected for analysis at 3 and 7 days post-ischemia.
  
  
  RESULTS
  Renal functional and structural recovery was markedly improved by POC, which increased the number of CXCR4(+) and CD34(+) stem cells in peripheral blood and kidney tissue. Inhibition of ROS burst by POC was likely associated with increased hypoxia-inducible factor-1 expression, which may further promote stromal cell-derived factor 1 (SDF-1) expression.
  
  
  CONCLUSIONS
  The mechanisms of stem cell recruitment to the injured foci mobilized by POC appear to be mediated by moderate oxidative stress, which may lead to increased SDF-1 expression.
authors: Key Laboratory of Biotechnology and Pharmaceutical Engineering, Molecular Pharmacology Research Center, School of Pharmacy, Wenzhou Medical University, Wenzhou, China.
authors: Xiaohua
authors: X
authors: Tan
authors: Ruili
authors: R
authors: Yin
authors: Yan
authors: Y
authors: Chen
authors: Dan
authors: D
authors: Gao
authors: Xiuying
authors: X
authors: Zhang
mesh_terms: D058186:Acute Kidney Injury / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D018952:Antigens, CD34 / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002465:Cell Movement; D054377:Chemokine CXCL12 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D019650:Hematopoietic Stem Cell Mobilization / Q000379:methods*; D006412:Hematopoietic Stem Cells / Q000378:metabolism / Q000473:pathology*; D051793:Hypoxia-Inducible Factor 1 / Q000235:genetics / Q000378:metabolism; D057775:Ischemic Postconditioning / Q000379:methods*; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D018384:Oxidative Stress; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000378:metabolism; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D013997:Time Factors
chemical_list: D018952:Antigens, CD34; D015415:Biomarkers; C575935:CXCL12 protein, rat; D054377:Chemokine CXCL12; C486264:Cxcr4 protein, rat; D051793:Hypoxia-Inducible Factor 1; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D019718:Receptors, CXCR4; D019009:Proto-Oncogene Proteins c-kit