Induced pluripotent stem cells without c-Myc attenuate acute kidney injury via downregulating the signaling of oxidative stress and inflammation in ischemia-reperfusion rats

Cell Transplant. 2012;21(12):2569-85. doi: 10.3727/096368912X636902. Epub 2012 Apr 10.

Abstract

Induced pluripotent stem (iPS) cells have potential for multilineage differentiation and provide a resource for stem cell-based treatment. However, the therapeutic effect of iPS cells on acute kidney injury (AKI) remains uncertain. Given that the oncogene c-Myc may contribute to tumorigenesis by causing genomic instability, herein we evaluated the therapeutic effect of iPS cells without exogenously introduced c-Myc on ischemia-reperfusion (I/R)-induced AKI. As compared with phosphate-buffered saline (PBS)-treated group, administration of iPS cells via intrarenal arterial route into kidneys improved the renal function and attenuated tubular injury score at 48 h after ischemia particularly at the dose of 5 × 10(5) iPS cells. However, a larger number of iPS cells (5 × 10(7) per rat) diminished the therapeutic effects for AKI and profoundly reduced renal perfusion detected by laser Doppler imaging in the reperfusion phase. In addition, the green fluorescence protein-positive iPS cells mobilized to the peritubular area at 48 h following ischemia, accompanied by a significant reduction in infiltration of macrophages and apoptosis of tubular cells, and a remarkable enhancement in endogenous tubular cell proliferation. Importantly, transplantation of iPS cells reduced the expression of oxidative substances, proinflammatory cytokines, and apoptotic factors in I/R kidney tissues and eventually improved survival in rats of ischemic AKI. Six months after transplantation in I/R rats, engrafted iPS cells did not result in tumor formation in kidney and other organs. In summary, considering the antioxidant, anti-inflammatory, and antiapoptotic properties of iPS cells without c-Myc, transplantation of such cells may be a treatment option for ischemic AKI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / complications
  • Acute Kidney Injury / mortality
  • Acute Kidney Injury / therapy*
  • Animals
  • Apoptosis
  • Blood Urea Nitrogen
  • Cell Differentiation
  • Cells, Cultured
  • Cytokines / metabolism
  • Down-Regulation
  • Induced Pluripotent Stem Cells / cytology
  • Induced Pluripotent Stem Cells / metabolism
  • Induced Pluripotent Stem Cells / transplantation*
  • Inflammation / metabolism
  • Inflammation / pathology*
  • Mice
  • Mice, Inbred C57BL
  • Oxidative Stress*
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / complications
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Signal Transduction
  • Survival Rate

Substances

  • Cytokines
  • Proto-Oncogene Proteins c-myc