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pubmed-article:21162127pubmed:abstractTextChemokines can be produced by gliomas, which mediate the infiltration of microglia, a characteristic feature of glioma-associated neuropathogenesis. ATP that is released at a high level from glioma has been reported to play a regulatory role in chemokine production in cultured glioma cells. The objective of this study was to define the potential role of extracellular ATP in the regulation of macrophage inflammatory protein-1? (MIP-1?) and monocyte chemoattractant protein-1(MCP-1) expression in glioma-associated microglia/macrophages. The results showed that Iba1(+) and ED1(+) microglia existed in the tumor at 3 and 7 day after injection of C6 glioma cells into the rat cerebral cortex (dpi). ED1(+) microglia/macrophages or Iba1(+) microglia in the glioma were also colocalized to MIP-1?- and MCP-1-expressing cells. In vitro study indicated that treatment with ATP and BzATP (an agonist for ATP ionotropic receptor P2X?R) caused an increase in the intracellular levels of microglial MIP-1? and MCP-1. By using an extracellular Ca(2+) chelator (EGTA) and P2X?R antagonists, oxidized ATP (oxATP) and brilliant blue G (BBG), we demonstrated that BzATP-induced production of MIP-1? and MCP-1 levels was due to P2X?R activation and Ca(2+) -dependent regulation. Coadministration of C6 glioma cells and oxATP into the rat cerebral cortex resulted in a reduction of MIP-1?- and MCP-1-expressing microglia/macrophages. We suggest, based on the results from in vivo and in vitro studies, that a massive amount of ATP molecules released in the glioma tumor site may act as the regulator with P2X?R signaling that increases MIP-1? and MCP-1 expression in tumor-infiltrating microglia/macrophages.lld:pubmed
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pubmed-article:21162127pubmed:copyrightInfoCopyright © 2010 Wiley-Liss, Inc.lld:pubmed
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pubmed-article:21162127pubmed:articleTitleExpression of macrophage inflammatory protein-1? and monocyte chemoattractant protein-1 in glioma-infiltrating microglia: involvement of ATP and P2X? receptor.lld:pubmed
pubmed-article:21162127pubmed:affiliationDepartment of Life Sciences, National Cheng Kung University, Tainan, Taiwan.lld:pubmed
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pubmed-article:21162127pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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