Acid-sensing by the T cell death-associated gene 8 (TDAG8) receptor cloned from rat brain

The T cell death-associated gene 8 (TDAG8) is a pH-sensing GPCR with a reported immune-specific expression profile. Here, we demonstrate pH-induced activation of TDAG8 receptor cloned from rodent brain (rTDAG8). Cloned rTDAG8 transcript showed 88–95% homology with human and mouse transcripts of lymp...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-08, Vol.386 (3), p.420-425
Main Authors: McGuire, Jennifer, Herman, James P., Ghosal, Sriparna, Eaton, Katherine, Sallee, Floyd R., Sah, Renu
Format: Article
Language:English
Subjects:
Acid-Base Equilibrium
Acid-sensing
Amino Acid Sequence
Animals
Brain Ischemia - metabolism
cAMP
Cell Survival
Cloning
Cloning, Molecular
Cyclic AMP - metabolism
Forebrain limbic
Hydrogen-Ion Concentration
Male
Molecular Sequence Data
Panic Disorder - metabolism
pCREB
pH-sensing
Prosencephalon - metabolism
Rats
Rats, Sprague-Dawley
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Signal Transduction
T cell death-associated gene 8
TDAG8
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Summary:The T cell death-associated gene 8 (TDAG8) is a pH-sensing GPCR with a reported immune-specific expression profile. Here, we demonstrate pH-induced activation of TDAG8 receptor cloned from rodent brain (rTDAG8). Cloned rTDAG8 transcript showed 88–95% homology with human and mouse transcripts of lymphoid origin. RT-PCR revealed high expression of TDAG8 in forebrain limbic regions. Extracellular acidification induced significantly elevated intracellular cyclic AMP, and phosphorylated CREB in TDAG8 expressing cells. Acidification-induced LDH release was significantly attenuated in cells expressing TDAG8, suggesting neuroprotective potential against acidosis-related cell injury. Our results open up new areas of investigation into the relevance of TDAG8 in pH homeostasis and pathological states associated with acid–base dys-regulation in the brain such as ischemia and panic disorder.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.05.133