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Signaling Mechanisms of Adenosine Action in Rat Brain Astrocytes
Author(s) -
Gebremedhin Debebe,
Rau Nicole,
Harder David R.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1094.9
Subject(s) - adenosine , neuroscience , action (physics) , astrocyte , chemistry , pharmacology , medicine , biology , physics , central nervous system , quantum mechanics
In the present study, we examined contribution of prominent signaling pathways in the adenosine receptor stimulation induced generation of superoxide, production or release of EETs and 20‐HETE from brain astrocytes using western blotting, fluorescent HPLC assay, and LC/MS analysis. Stimulation of brain astrocytes with adenosine or with the A 2a adenosine receptor agonist CGS‐21680, induced an increase in Akt phosphorylation mediated by the A 2a receptor subtype, which was independent of coupling with the adenosine releasable second messengers cAMP and cGMP. Stimulation of astrocytes with either cAMP or cGMP did not change level of superoxide generation and production or release of EETs or 20‐HETE. Stimulation of the A2a and A2b adenosine receptor subtypes induced activation of p38 MAPK that was augmented following specific inhibition of the PI3K pathway, suggesting that Akt phosphorylation may be a negative regulator of p38 MAPK activation by adenosine receptor stimulation. It is concluded that the A2a and A2b adenosine receptor subtype stimulation is coupled to AKt phosphorylation, and that the second messengers cAMP and cGMP are not contributing to the adenosine induced superoxide generation or production or release of EETs or 20‐HETE from brain astrocytes.