Macrophages regulate smooth muscle differentiation of mesenchymal stem cells via a prostaglandin F₂α-mediated paracrine mechanism

Arterioscler Thromb Vasc Biol. 2012 Nov;32(11):2733-40. doi: 10.1161/ATVBAHA.112.300230. Epub 2012 Sep 6.

Abstract

Objective: Mesenchymal stem cells are useful for vascular regeneration of injured tissues. Macrophages are involved in acute or chronic inflammatory diseases, and interleukin-1β (IL-1β), a proinflammatory cytokine, plays a key role in the activation of macrophages within injured tissues. To explore the role of macrophages on mesenchymal stem cell-mediated vascular regeneration, we examined the effects of IL-1β-activated macrophages on differentiation of human adipose tissue-derived mesenchymal stem cells (hASCs) to smooth muscle cells (SMCs) and the vascular regenerative capacity of the differentiated SMCs in a hindlimb ischemia animal model.

Methods and results: We demonstrate that IL-1β-conditioned medium from RAW 264.7 macrophages induces differentiation of human adipose tissue-derived mesenchymal stem cells to α-smooth muscle actin-positive SMCs, and the differentiated SMCs exhibited increased contractility in response to KCl and carbachol treatment. Transplantation of the differentiated SMCs attenuated severe hindlimb ischemia and promoted vascular regeneration. IL-1β treatment stimulated secretion of prostaglandin F(2α) from RAW 264.7 cells. Small interfering RNA-mediated silencing of the prostaglandin F(2α) receptor completely abrogated IL-1β conditioned medium-stimulated α-smooth muscle actin expression. Moreover, prostaglandin F(2α) treatment stimulated expression of α-smooth muscle actin in human adipose tissue-derived mesenchymal stem cells.

Conclusions: These results suggest that IL-1β-activated macrophages promote differentiation of human adipose tissue-derived mesenchymal stem cells to SMCs through a prostaglandin F(2α)-mediated paracrine mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Adipose Tissue / cytology
  • Animals
  • Biomarkers / metabolism
  • Cell Differentiation*
  • Cell Line
  • Coculture Techniques
  • Culture Media, Conditioned / metabolism
  • Dinoprost / metabolism*
  • Disease Models, Animal
  • Hindlimb
  • Humans
  • Inflammation Mediators / metabolism
  • Interleukin-1beta / metabolism
  • Ischemia / immunology
  • Ischemia / metabolism
  • Ischemia / physiopathology
  • Ischemia / surgery
  • Macrophage Activation
  • Macrophages / immunology
  • Macrophages / metabolism*
  • Mesenchymal Stem Cell Transplantation
  • Mesenchymal Stem Cells / immunology
  • Mesenchymal Stem Cells / metabolism*
  • Mice
  • Mice, Nude
  • Muscle, Skeletal / blood supply*
  • Myocytes, Smooth Muscle / immunology
  • Myocytes, Smooth Muscle / metabolism*
  • Myocytes, Smooth Muscle / transplantation
  • Neovascularization, Physiologic
  • Paracrine Communication*
  • RNA Interference
  • Receptors, Prostaglandin / genetics
  • Receptors, Prostaglandin / metabolism
  • Regional Blood Flow
  • Time Factors
  • Transfection

Substances

  • ACTA2 protein, human
  • Actins
  • Biomarkers
  • Culture Media, Conditioned
  • Inflammation Mediators
  • Interleukin-1beta
  • Receptors, Prostaglandin
  • prostaglandin F2alpha receptor
  • Dinoprost