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Adenosine A 3 receptor‐induced CCL2 synthesis in cultured mouse astrocytes
Author(s) -
Wittendorp Maria C.,
Boddeke Hendrikus W.G.M.,
Biber Knut
Publication year - 2004
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20016
Subject(s) - adenosine , adenosine receptor , neuroprotection , adenosine a1 receptor , biology , purinergic signalling , agonist , adenosine a3 receptor , receptor , stimulation , adenosine a2b receptor , pharmacology , neuroglia , astrocyte , microbiology and biotechnology , endocrinology , medicine , biochemistry , central nervous system
During neuropathological conditions, high concentrations of adenosine are released, stimulating adenosine receptors in neurons and glial cells. It has recently been shown that stimulation of adenosine receptors in glial cells induces the release of neuroprotective substances such as NGF, S‐100β, and interleukin‐6 (IL‐6). It has therefore been suggested that glial adenosine receptors are involved in neuroprotection. Since recently neuroprotective effects of the chemokine CCL2 (formerly known as MCP‐1) have been reported, we investigated the possible effect of adenosine receptor stimulation on glial CCL2 synthesis. Here we show that stimulation of cultured murine astrocytes with the selective adenosine A 3 receptor agonist 2‐chloro‐N6‐(3‐iodobenzyl)‐N‐methyl‐5′‐carbamoyladenosine (CL‐IB‐MECA) induced the release of CCL2. Specific ligands for adenosine A 1 or A 2 receptors did not affect CCL2 release. Furthermore, CL‐IB‐MECA‐induced CCL2 synthesis was inhibited by adenosine A 3 receptor antagonists. These results show that stimulation of adenosine A 3 receptors in astrocytes induced the release of CCL2, thus supporting the assumption that adenosine receptors in glial cells regulate the synthesis of neuroprotective substances. © 2004 Wiley‐Liss, Inc.