Repair of acute myocardial infarction by human stemness factors induced pluripotent stem cells

Circulation. 2009 Aug 4;120(5):408-16. doi: 10.1161/CIRCULATIONAHA.109.865154. Epub 2009 Jul 20.

Abstract

Background: Nuclear reprogramming provides an emerging strategy to produce embryo-independent pluripotent stem cells from somatic tissue. Induced pluripotent stem cells (iPS) demonstrate aptitude for de novo cardiac differentiation, yet their potential for heart disease therapy has not been tested.

Methods and results: In this study, fibroblasts transduced with human stemness factors OCT3/4, SOX2, KLF4, and c-MYC converted into an embryonic stem cell-like phenotype and demonstrated the ability to spontaneously assimilate into preimplantation host morula via diploid aggregation, unique to bona fide pluripotent cells. In utero, iPS-derived chimera executed differentiation programs to construct normal heart parenchyma patterning. Within infarcted hearts in the adult, intramyocardial delivery of iPS yielded progeny that properly engrafted without disrupting cytoarchitecture in immunocompetent recipients. In contrast to parental nonreparative fibroblasts, iPS treatment restored postischemic contractile performance, ventricular wall thickness, and electric stability while achieving in situ regeneration of cardiac, smooth muscle, and endothelial tissue.

Conclusions: Fibroblasts reprogrammed by human stemness factors thus acquire the potential to repair acute myocardial infarction, establishing iPS in the treatment of heart disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Adult Stem Cells / cytology*
  • Adult Stem Cells / physiology
  • Animals
  • Cell Dedifferentiation / physiology
  • Fibroblasts / cytology
  • Fibroblasts / physiology
  • Genes, myc
  • Genetic Vectors
  • Heart / embryology
  • Humans
  • Kruppel-Like Factor 4
  • Kruppel-Like Transcription Factors / genetics
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Nude
  • Myocardial Infarction / pathology*
  • Myocardial Infarction / therapy*
  • Octamer Transcription Factor-3 / genetics
  • Pluripotent Stem Cells / cytology*
  • Pluripotent Stem Cells / physiology
  • Recovery of Function
  • SOXB1 Transcription Factors / genetics
  • Stem Cell Transplantation / methods*
  • Transduction, Genetic

Substances

  • KLF4 protein, human
  • Klf4 protein, mouse
  • Kruppel-Like Factor 4
  • Kruppel-Like Transcription Factors
  • Octamer Transcription Factor-3
  • POU5F1 protein, human
  • SOX2 protein, human
  • SOXB1 Transcription Factors