Purines are important modulators of bone cell biology. ATP is metabolized into adenosine by human primary osteoblast cells (HPOC); due to very low activity of adenosine deaminase, the nucleoside is the end product of the ecto‐nucleotidase cascade. We, therefore, investigated the expression and function of adenosine receptor subtypes (A1, A2A, A2B, and A3) during proliferation and osteogenic differentiation of HPOC. Adenosine A1 (CPA), A2A (CGS21680C), A2B (NECA), and A3 (2‐Cl‐IB‐MECA) receptor agonists concentration‐dependently increased HPOC proliferation. Agonist‐induced HPOC proliferation was prevented by their selective antagonists, DPCPX, SCH442416, PSB603, and MRS1191. CPA and NECA facilitated osteogenic differentiation measured by increases in alkaline phosphatase (ALP) activity. This contrasts with the effect of CGS21680C which delayed HPOC differentiation; 2‐Cl‐IB‐MECA was devoid of effect. Blockade of the A2B receptor with PSB603 prevented osteogenic differentiation by NECA. In the presence of the A1 antagonist, DPCPX, CPA reduced ALP activity at 21 and 28 days in culture. At the same time points, blockade of A2A receptors with SCH442416 transformed the inhibitory effect of CGS21680C into facilitation. Inhibition of adenosine uptake with dipyridamole caused a net increase in osteogenic differentiation. The presence of all subtypes of adenosine receptors on HPOC was confirmed by immunocytochemistry. Data show that adenosine is an important regulator of osteogenic cell differentiation through the activation of subtype‐specific receptors. The most abundant A2B receptor seems to have a consistent role in cell differentiation, which may be balanced through the relative strengths of A1 or A2A receptors determining whether osteoblasts are driven into proliferation or differentiation. J. Cell. Physiol. 226: 1353–1366, 2011. © 2010 Wiley‐Liss, Inc.
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On the role of subtype selective adenosine receptor agonists during proliferation and osteogenic differentiation of human primary bone marrow stromal cells
Costa, M. Adelina; Barbosa, A.; Neto, E.; Sá‐e‐Sousa, A.; Freitas, R.; Neves, J.M.; Magalhães‐Cardoso, T.; Ferreirinha, F.; Correia‐de‐Sá, P.
Follow Journal of Cellular Physiology
, Volume 226 (5)
Wiley – May 1, 2011
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