Renoprotective effect of human umbilical cord-derived mesenchymal stem cells in immunodeficient mice suffering from acute kidney injury

PLoS One. 2012;7(9):e46504. doi: 10.1371/journal.pone.0046504. Epub 2012 Sep 27.

Abstract

It is unknown whether human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) can improve the renal function of patients suffering from acute kidney injury. Moreover, before beginning clinical trials, it is necessary to investigate this renoprotective effect of hUC-MSCs in a xenogeneic model of acute kidney injury. However, no previous studies have examined the application of hUC-MSCs to immunodeficient mice suffering from acute kidney injury. The objectives of this study were to examine whether hUC-MSCs could improve renal function in nonobese diabetic-severe combined immune deficiency (NOD-SCID) mice suffering from acute kidney injury, and to investigate the mechanism(s) for hUC-MSCs to improve renal function in this xenogeneic model. Early (3 hr) and late (12 hr) administrations of hUC-MSCs (10(6) cells) were performed via the external jugular vein into NOD-SCID mice suffering from either folic acid (FA) (250 mg/kg body weight) or vehicle. The results showed that early administration of hUC-MSCs improved the renal function of NOD-SCID mice suffering from FA-induced acute kidney injury, as evidenced by decreased serum urea nitrogen and serum creatinine levels, as well as a reduced tubular injury score. The beneficial effects of hUC-MSCs were through reducing apoptosis and promoting proliferation of renal tubular cells. These benefits were independent of inflammatory cytokine effects and transdifferentiation. Furthermore, this study is the first one to show that the reduced apoptosis of renal tubular cells by hUC-MSCs in this xenogeneic model is mediated through the mitochondrial pathway, and through the increase of Akt phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / blood
  • Acute Kidney Injury / chemically induced
  • Acute Kidney Injury / therapy*
  • Animals
  • Antigens, CD / metabolism
  • Apoptosis
  • Blood Urea Nitrogen
  • Caspases / metabolism
  • Cell Differentiation
  • Cell Proliferation
  • Creatinine / blood
  • Cytokines / metabolism
  • Cytoprotection
  • Folic Acid
  • Humans
  • Inflammation Mediators / metabolism
  • Insulin-Like Growth Factor I / metabolism
  • Kidney Tubules / metabolism
  • Kidney Tubules / pathology
  • Kidney Tubules / physiopathology
  • Male
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / metabolism
  • Mesenchymal Stem Cells / physiology*
  • Mice
  • Mice, Inbred NOD
  • Mice, SCID
  • Tissue Array Analysis
  • Umbilical Cord / cytology
  • Wharton Jelly / cytology*

Substances

  • Antigens, CD
  • Cytokines
  • Inflammation Mediators
  • Insulin-Like Growth Factor I
  • Folic Acid
  • Creatinine
  • Caspases

Grants and funding

This study was supported by research grants from the National Science Council, Taiwan (NSC 95-2745-B-303-001) to TCF, and from the Tzu Chi General Hospital, Hualien, Taiwan (TCRD 98-24 and TCRD 99-17) to TCF. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No additional external funding was received for this study.