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Activation of P2X7 receptor can lead to NAD+ release from astrocytes
Author(s) -
Ying Weihai,
Xia Weiliang,
Chen Heyu
Publication year - 2010
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.24.1_supplement.962.11
Subject(s) - nad+ kinase , extracellular , ppads , intracellular , agonist , microbiology and biotechnology , biology , purinergic receptor , chemistry , receptor , pharmacology , biochemistry , enzyme
NAD+ plays critical roles in various biological processes. Recent studies have also suggested that extracellular NAD+ can induce death of a certain population of T cells, while there has been no information regarding the pathways by which intracellular NAD+ can be released into extracellular space. In this study we tested our hypothesis that activation of P2X7 receptors (P2X7R) can lead to NAD+ release from astrocytes. We found that the selective P2X7R agonist bzATP produced dose‐dependent decreases in intracellular NAD+ as well as increases in extracellular NAD+. The BzATP‐induced NAD+ loss was significantly attenuated by the P2 receptor antagonists PPADS and suramin, and completely blocked by the P2X7R antagonist oxATP. RNA silencing‐produced P2X7R reductions also led to prevention of the BzATP‐induced NAD+ release. Collectively, our results provide the first evidence demonstrating that NAD+ can be released from activated P2X7R, at least in such cell types as astrocytes (Supported by a Key Research Grant of Shanghai Municipal Scientific Committee, Pujiang Scholar Program Grant, Shanghai Engineering Center Grant of Equipment and Technology of Physical Therapy for Major Diseases, and a Shanghai Rising‐Star Program Grant).