Abstract
Adenosine signals via the A2b adenosine receptor (A2bAR) to activate adenylyl cyclase. Previously we found that mesenchymal stem cells, precursors to osteoblasts and adipocytes, from A2bAR knockout (KO) mice have reduced capacity for osteoblast differentiation. Thus, we hypothesized that the A2bAR regulates adipogenesis. The stromal‐vascular fraction of mouse fat, which contains adipocyte progenitors, was induced to differentiate into adipocytes. We found that the expression of the A2bAR decreases substantially during adipogenesis. Bay 60–6583, an A2bAR specific agonist, inhibits adipocyte differentiation as shown by reduction in expression of fat differentiation markers and the number of mature adipocytes. In search for mechanisms, a novel link was identified between A2bAR signaling and upregulation of the stem cell factor, KLF4, in association with cellular proliferation. Adipocyte precursor proliferation in A2bAR KO mice differed from wild type mice following high fat diet feeding as visualized by in vivo BrdU labeling. These findings demonstrate a novel function of the A2bAR in adipocyte differentiation and positions this receptor as an important mediator of stem cell fate.
Published Version
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