Insulin-like growth factor promotes cardiac lineage induction in vitro by selective expansion of early mesoderm

Stem Cells. 2014 Jun;32(6):1493-502. doi: 10.1002/stem.1660.

Abstract

A thorough understanding of the developmental signals that direct pluripotent stem cells (PSCs) toward a cardiac fate is essential for translational applications in disease modeling and therapy. We screened a panel of 44 cytokines/signaling molecules for their ability to enhance Nkx2.5(+) cardiac progenitor cell (CPC) formation during in vitro embryonic stem cell (ESC) differentiation. Treatment of murine ESCs with insulin or insulin-like growth factors (IGF1/2) during early differentiation increased mesodermal cell proliferation and, consequently, CPC formation. Furthermore, we show that downstream mediators of IGF signaling (e.g., phospho-Akt and mTOR) are required for this effect. These data support a novel role for IGF family ligands to expand the developing mesoderm and promote cardiac differentiation. Insulin or IGF treatment could provide an effective strategy to increase the PSC-based generation of CPCs and cardiomyocytes for applications in regenerative medicine.

Keywords: Akt; Cardiac differentiation; Cardiac progenitor cell; Cardiomyocyte; Development; Embryonic stem cell; In vitro screening; Insulin; Insulin-like growth factor; Mesoderm.

Publication types

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

MeSH terms

  • Animals
  • Cell Differentiation / drug effects
  • Cell Line
  • Cell Lineage / drug effects*
  • Cell Proliferation / drug effects
  • Embryonic Stem Cells / metabolism
  • Fetal Proteins / metabolism
  • Gene Expression Regulation, Developmental / drug effects
  • Insulin
  • Insulin-Like Growth Factor I / pharmacology*
  • Insulin-Like Growth Factor II / pharmacology*
  • Mesoderm / cytology*
  • Mesoderm / drug effects
  • Mesoderm / embryology
  • Mesoderm / metabolism
  • Mice
  • Myocardium / cytology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphoinositide-3 Kinase Inhibitors
  • Phosphorylation / drug effects
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects
  • Stem Cells / cytology
  • Stem Cells / drug effects
  • Stem Cells / metabolism
  • T-Box Domain Proteins / metabolism
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Fetal Proteins
  • Insulin
  • Phosphoinositide-3 Kinase Inhibitors
  • T-Box Domain Proteins
  • Insulin-Like Growth Factor I
  • Insulin-Like Growth Factor II
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • Brachyury protein