Adenosine receptor subtype expression and activation influence the differentiation of mesenchymal stem cells to osteoblasts and adipocytes

J Bone Miner Res. 2011 Sep;26(9):2112-24. doi: 10.1002/jbmr.424.

Abstract

Osteoblasts and adipocytes differentiate from a common precursor cell, the mesenchymal stem cell (MSC). Adenosine is known to signal via four adenosine receptor subtypes, and significantly, recent findings indicate that these may play a role in MSC differentiation. We therefore investigated adenosine receptor expression and activation during the differentiation of MSCs to osteoblasts and adipocytes. The A(2B) R was dominant in MSCs, and its expression and activity were transiently upregulated at early stages of osteoblastic differentiation. Both activation and overexpression of A(2B) R induced the expression of osteoblast-related genes [Runx2 and alkaline phosphatase (ALP)], as well as ALP activity, and stimulation increased osteoblast mineralization. The expression of A(2A) R was upregulated during later stages of osteoblastic differentiation, when its activation stimulated ALP activity. Differentiation of MSCs to adipocytes was accompanied by significant increases in A(1) R and A(2A) R expression, and their activation was associated with increased adipogenesis. Enhanced A(2A) R expression was sufficient to promote expression of adipocyte-related genes (PPARγ and C/EBPα), and its activation resulted in increased adipocytic differentiation and lipid accumulation. In contrast, the A(1) R was involved mainly in lipogenic activity of adipocytes rather than in their differentiation. These results show that adenosine receptors are differentially expressed and involved in lineage-specific differentiation of MSCs. We conclude, therefore, that fruitful strategies for treating diseases associated with an imbalance in the differentiation and function of these lineages should include targeting adenosine receptor signal pathways. Specifically, these research avenues will be useful in preventing or treating conditions with insufficient bone or excessive adipocyte formation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine-5'-(N-ethylcarboxamide) / pharmacology
  • Adipocytes / cytology*
  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipogenesis / drug effects
  • Adipogenesis / genetics
  • Alkaline Phosphatase / metabolism
  • Animals
  • Biomarkers / metabolism
  • Blotting, Western
  • Calcification, Physiologic / drug effects
  • Calcification, Physiologic / genetics
  • Cell Count
  • Cell Differentiation* / genetics
  • Cyclic AMP / metabolism
  • Gene Expression Regulation / drug effects
  • Humans
  • Lipid Metabolism / drug effects
  • Mesenchymal Stem Cells / cytology*
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / metabolism
  • Osteoblasts / cytology*
  • Osteoblasts / drug effects
  • Osteoblasts / enzymology
  • Osteogenesis / drug effects
  • Osteogenesis / genetics
  • Purinergic P1 Receptor Agonists / pharmacology
  • Purinergic P1 Receptor Antagonists / pharmacology
  • Rats
  • Receptors, Purinergic P1 / genetics
  • Receptors, Purinergic P1 / metabolism*
  • Signal Transduction / drug effects

Substances

  • Biomarkers
  • Purinergic P1 Receptor Agonists
  • Purinergic P1 Receptor Antagonists
  • Receptors, Purinergic P1
  • Adenosine-5'-(N-ethylcarboxamide)
  • Cyclic AMP
  • Alkaline Phosphatase