TGF-α equalizes age disparities in stem cell-mediated cardioprotection

J Surg Res. 2012 Aug;176(2):386-94. doi: 10.1016/j.jss.2011.11.1012. Epub 2011 Dec 14.

Abstract

Background: Neonatal mesenchymal stem cells exhibit less cardioprotective potential than their adult counterparts. Transforming growth factor-α (TGF-α) has been shown to stimulate adult stem cell VEGF production, however, it remains unknown whether it may augment neonatal stem cell paracrine function. We hypothesized that TGF-α would equalize adult and neonatal stem cell paracrine function and cardioprotection during acute ischemia/reperfusion.

Materials and methods: Bone marrow mesenchymal stem cells isolated from adult and 2.5 wk-old mice were treated with TGF-α (250 ng/mL) for 24 h. VEGF, HGF, IGF-1, IL-1β, and IL-6 production were measure in vitro, and cells were infused via an intracoronary route using a model of isolated heart perfusion.

Results: TGF-α equalized adult and neonatal stem cell VEGF production but did not affect production of HGF, IGF-1, IL-1β, or IL-6. ERK, p38 MAPK, and JNK phosphorylation were greater in adult cells in response to TGF-α. Whereas infusion of adult but not neonatal stem cells was associated with improved myocardial functional recovery during reperfusion, infusions of either TGF-α-pretreated cell group were associated with the greatest functional recovery. TGF-α equalizes adult and neonatal mesenchymal stem cell VEGF production and cardioprotection in association with differential regulation of ERK, p38 MAPK, and JNK phosphorylation.

MeSH terms

  • Acute Disease
  • Adult Stem Cells / cytology
  • Adult Stem Cells / drug effects*
  • Adult Stem Cells / metabolism
  • Age Factors
  • Animals
  • Animals, Newborn
  • Caspase 3 / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Signaling System / physiology
  • Male
  • Mesenchymal Stem Cell Transplantation / methods*
  • Mesenchymal Stem Cells / cytology
  • Mesenchymal Stem Cells / drug effects*
  • Mesenchymal Stem Cells / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / therapy*
  • Myocardium / cytology
  • Myocardium / metabolism
  • Paracrine Communication / drug effects
  • Paracrine Communication / physiology
  • Transforming Growth Factor alpha / metabolism
  • Transforming Growth Factor alpha / pharmacology*
  • Tumor Necrosis Factor-alpha / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Interleukin-1beta
  • Interleukin-6
  • Transforming Growth Factor alpha
  • Tumor Necrosis Factor-alpha
  • Extracellular Signal-Regulated MAP Kinases
  • JNK Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Casp3 protein, mouse
  • Caspase 3