Journal
GLIA
Volume 56, Issue 3, Pages 331-341Publisher
WILEY
DOI: 10.1002/glia.20606
Keywords
microglia; purinergic receptors type 2; migration; ATP; cd39; ENTPDase; brain
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Funding
- NHLBI NIH HHS [R01 HL063972-08, R01 HL063972] Funding Source: Medline
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Microglia is activated by brain injury. They migrate in response to ATP and although adenosine alone has no effect on wild type microglial migration, we show that inhibition of adenosine receptors impedes ATP triggered migration. CD39 is the dominant cellular ectonucleotidase that degrades nucleotides to nucleosides, including adenosine. Importantly, ATP fails to stimulate P2 receptor mediated migration in cd39(-/-) microglia. However, the effects of ATP on migration in cd39(-/-) microglia can be restored by co-stimulation with adenosine or by addition of a soluble ectonucleotidase. We also tested the impact of cd39-deletion in a model of ischemia, in an entorhinal cortex lesion and in the facial nucleus after facial nerve lesion. The accumulation of microglia at the pathological sites was markedly decreased in cd39(-/-) animals. We conclude that the co-stimulation of purinergic and adenosine receptors is a requirement for microglial migration and that the expression of cd39 controls the ATP/adenosine balance. (C) 2007 Wiley-Liss, Inc.
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