title: Mesenchymal stem cells, not conditioned medium, contribute to kidney repair after ischemia-reperfusion injury.
abstract: BACKGROUND
  Studies have shown that stem cells exert their therapeutic effects on acute kidney injury (AKI) through paracrine/endocrine actions. If the protective effect is mediated in an endocrine manner, the injection of the factors that these cells secrete could be effective, but the effect of conditioned medium (CM) remains controversial.
  
  
  METHODS
  In this study, we cultured mesenchymal stem cells (MSCs) and then transplanted them into an ischemia-reperfusion (I/R) injury model. CM was also injected into mice, and the histological changes, level of cell proliferation, loss of peritubular capillaries and anti-inflammatory and anti-apoptotic effects were examined at different time points.
  
  
  RESULTS
  The results showed that MSC infusion improved renal function and histological alterations, leading to significantly reduced mortality. MSC administration also promoted kidney microvasculature repair, attenuated kidney peritubular capillary loss, increased the proliferation of parenchymal cells and decreased CD68-positive macrophage infiltration and apoptotic cells. Although we determined that CM contained proangiogenic factors, including hepatocyte growth factor (HGF), vascular endothelial growth factor-A (VEGF-A) and insulin-like growth factor-1 (IGF-1), no favorable effects were observed during the course of repair.
  
  
  CONCLUSIONS
  Our data show that MSC infusion promotes kidney repair in a variety of ways, including enhancement of the repair of peritubular capillaries and tubular epithelial cells and anti-inflammatory and anti-apoptotic effects. MSCs can secrete high levels of proangiogenic growth factors, but CM results in a nonsignificant improvement, indicating that MSCs play a role in kidney repair through paracrine rather than endocrine mechanisms. These results indicate that MSC infusion is a promising therapeutic strategy for promoting kidney repair after injury.
authors.forename: Li
authors.initials: L
authors.lastname: Xing
authors.forename: Rui
authors.initials: R
authors.lastname: Cui
authors.forename: Lei
authors.initials: L
authors.lastname: Peng
authors.forename: Jing
authors.initials: J
authors.lastname: Ma
authors.forename: Xiao
authors.initials: X
authors.lastname: Chen
authors.forename: Ru-Juan
authors.initials: RJ
authors.lastname: Xie
authors.forename: Bing
authors.initials: B
authors.lastname: Li
mesh_terms: D058186:Acute Kidney Injury / Q000473:pathology / Q000628:therapy*; D000818:Animals; D017209:Apoptosis; D018929:Cell Culture Techniques; D049109:Cell Proliferation; D064987:Cell- and Tissue-Based Therapy; D017077:Culture Media, Conditioned / Q000494:pharmacology*; D017228:Hepatocyte Growth Factor; D007334:Insulin-Like Growth Factor I; D008297:Male; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000166:cytology*; D008807:Mice, Inbred BALB C; D015427:Reperfusion Injury / Q000473:pathology / Q000628:therapy*; D042461:Vascular Endothelial Growth Factor A
chemical_list: D017077:Culture Media, Conditioned; D042461:Vascular Endothelial Growth Factor A; D017228:Hepatocyte Growth Factor; D007334:Insulin-Like Growth Factor I