Expression of mRNA for adenosine receptor subtypes A(1), A(2a), A(2b), and A(3) in normal and lipopolysaccharide (LPS)-activated murine RAW 264.7 macrophages has been investigated using the method of quantitative real-time polymerase chain reaction. The results have shown a very low, unquantifiable expression of adenosine A(1) receptor mRNA in both normal and LPS-activated macrophages. The other three adenosine receptor mRNAs have been found to be expressed at various but always quantifiable levels. Activation of the macrophages by LPS induced upregulation of the expression of adenosine receptor A(2a) and A(2b) mRNA, whereas the expression of adenosine receptor A(3) mRNA was downregulated. Unstimulated macrophages exhibited a high expression of the A(2b) adenosine receptor mRNA. The findings are discussed from the point of view of the antiinflammatory and hematopoiesis-stimulating roles of the adenosine receptor signaling.

• MeSH
• aktivace makrofágů genetika   účinky léků   MeSH
• buněčné linie MeSH
• časové faktory MeSH
• financování organizované MeSH
• hematopoéza genetika   účinky léků   MeSH
• lipopolysacharidy farmakologie   MeSH
• makrofágy metabolismus   účinky léků   MeSH
• messenger RNA metabolismus   MeSH
• myši MeSH
• polymerázová řetězová reakce MeSH
• purinergní receptory P1 genetika   účinky léků   MeSH
• receptor adenosinový A1 genetika   MeSH
• receptor adenosinový A2A genetika   MeSH
• receptor adenosinový A2B genetika   MeSH
• receptor adenosinový A3 genetika   MeSH
• regulace genové exprese MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH

Four mouse bone marrow or thymus cell populations, namely granulopoietic/monocytopoietic, erythropoietic, B-lymphopoietic, and T-lymphopoietic precursor cells have been assayed by RT-PCR technique for the presence and relative amounts of adenosine A(1), A(2a), A(2b), and A(3) receptor mRNA. It has been found that (i) all four populations studied express all four adenosine receptor subtypes, (ii) the A(1), receptor is the least expressed in all populations studied, (iii) the A(3) receptor is markedly expressed in the populations of granulopoietic/monocytopoietic and erythropoietic cells, (iv) the A(2a) receptor is markedly expressed in the populations of B-lymphopoietic and T-lymphopoietic cells, and v) the A(2b) receptor does not predominate in any of the precursor cells studied. Our data offer a new possibility for the assessment of the readiness of these cells to respond, by receptor-mediated mechanisms, to adenosine or its analogs present in the tissues as a result of endogenous processes and/or following their administration.

• MeSH
• financování organizované MeSH
• hematopoetické kmenové buňky metabolismus   MeSH
• hematopoéza genetika   MeSH
• messenger RNA metabolismus   MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• polymerázová řetězová reakce MeSH
• purinergní receptory P1 genetika   MeSH
• receptor adenosinový A1 genetika   MeSH
• receptor adenosinový A2A genetika   MeSH
• receptor adenosinový A2B genetika   MeSH
• receptor adenosinový A3 genetika   MeSH
• regulace genové exprese MeSH
• separace buněk MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH

Adenosine has been observed to suppress the growth of MOLT-4 human leukemia cells in vitro. Changes in the cell cycle, especially increased percentage of cells in S phase, prolonged generation time, and induction of apoptosis at higher adenosine concentrations have been found to be responsible for the growth suppression. Dipyridamole, a drug inhibiting the cellular uptake of adenosine, reversed partially but significantly the adenosine-induced growth suppression. It follows from these results that the action of adenosine on the MOLT-4 cells comprises its cellular uptake and intracellular operation. These findings present new data on anticancer efficacy of adenosine.

• MeSH
• adenosin antagonisté a inhibitory   farmakologie   metabolismus   MeSH
• apoptóza MeSH
• biologický transport účinky léků   MeSH
• dipyridamol farmakologie   MeSH
• financování organizované MeSH
• inhibitory fosfodiesteras farmakologie   MeSH
• leukemie T-buněčná patologie   MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• proliferace buněk účinky léků   MeSH
• protinádorové látky antagonisté a inhibitory   farmakologie   metabolismus   MeSH
• Check Tag
• lidé MeSH