Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways.

Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways. Research Abstract Details 

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Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways. Abstract Text:

N-O Hermansson,D G A Morgan,T Drmota,N Larsson,N-O Hermansson,D G A Morgan,T Drmota,N Larsson,

AIM: To assess if adenosine is a direct growth hormone secretagogue receptor (GHSR) agonist by investigating the mechanism behind adenosine induced calcium release in human embryonic kidney 293s (HEK) cells expressing GHSR. METHODS: Calcium mobilization, cyclic adenosine monophosphate (cAMP) and IP(3) experiments were performed using HEK cells stably expressing GHSR and/or adenosine A(2B) receptor (A(2B)R). RESULTS: Adenosine has been widely reported as a GHSR agonist. In our hands, adenosine and forskolin stimulated calcium release from IP(3) controlled stores in HEK-GHSR cells but not in non-transfected HEK cells. This release was not accompanied by increased IP(3) levels. The calcium release was both cholera toxin and U73122 sensitive, indicating the involvement of both Galpha(s)/adenylyl cyclase and Galpha(q/11)/phospholipase C pathways. Importantly, the GHSR inverse agonist [D-Arg(1) D-Phe(5) D-Trp(7,9) Leu(11)]-Substance P (SP-analogue) blocked the adenosine stimulated calcium release, demonstrating that GHSR is involved. Assessment of the GHSR-dependent calcium release using adenosine receptor agonists and antagonists resulted in a rank order of potencies resembling the profile of A(2B)R. A(2B)R over-expression in HEK-GHSR cells enhanced potency and efficacy of the adenosine induced calcium release without increasing IP(3) production. Moreover, A(2B)R over-expression in HEK cells potentiated NECA-induced cAMP production. However, GHSR expression had no effect on intracellular cAMP production. CONCLUSION: In HEK-GHSR cells adenosine activates endogenously expressed A(2B)R resulting in calcium mobilization. We hypothesize that the responsible mechanism is cAMP-dependent sensitization of IP(3) receptors for the high basal level of IP(3) caused by GHSR constitutive activity. Altogether, our results demonstrate that adenosine is not a direct GHSR agonist.

Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways. Publishing Authors By Initials

NO Hermansson,DG Morgan,T Drmota,N Larsson,NO Hermansson,DG Morgan,T Drmota,N Larsson,

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Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Acta physiologica (Oxford, England)

VOLUME: 190

Page Numbers: 77-86

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ISSN: 1748-1708

DAY: 12

MONTH: May

YEAR: 2007

Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Adenosine is not a direct GHSR agonist--artificial cross-talk between GHSR and adenosine receptor pathways.

AFFILIATION: Department of Lead Generation, AstraZeneca R&D Mölndal, Mölndal, Sweden.

Country: England

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MEDLINETA: Acta Physiol (Oxf)

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