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Coordination of agonist-induced Ca2+-signalling patterns by NAADP in pancreatic acinar cells

Author

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  • Jose Manuel Cancela

    (Mansfield Road, University of Oxford)

  • Grant C. Churchill

    (University of Liverpool)

  • Antony Galione

    (University of Liverpool)

Abstract

Many hormones and neurotransmitters evoke Ca2+ release fromintracellular stores, often triggering agonist-specific signatures of intracellular Ca2+ concentration1,2,3,4,5. Inositol trisphosphate (InsP3)1 and cyclic adenosine 5′-diphosphate-ribose (cADPR)6,7 are established Ca2+-mobilizing messengers that activate Ca2+ release through intracellular InsP3 and ryanodine receptors, respectively8,9,10. However, in pancreatic acinar cells, neither messenger can explain the complex pattern of Ca2+ signals triggered by the secretory hormone cholecystokinin (CCK). We show here that the Ca2+-mobilizing molecule nicotinic acid adenine dinucleotide phosphate (NAADP)7,11,12,13,14,15, an endogenous metabolite of β-NADP, triggers a Ca2+ response that varies from short-lasting Ca2+ spikes to a complex mixture of short-lasting (1–2 s) and long-lasting (0.2–1 min) Ca2+ spikes. Cells were significantly more sensitive to NAADP than to either cADPR or InsP3, whereas higher concentrations of NAADP selectively inactivated CCK-evoked Ca2+ signals in pancreatic acinar cells, indicating that NAADP may function as an intracellular messenger in mammalian cells.

Suggested Citation

  • Jose Manuel Cancela & Grant C. Churchill & Antony Galione, 1999. "Coordination of agonist-induced Ca2+-signalling patterns by NAADP in pancreatic acinar cells," Nature, Nature, vol. 398(6722), pages 74-76, March.
    • Handle: RePEc:nat:nature:v:398:y:1999:i:6722:d:10.1038_18032
    DOI: 10.1038/18032
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    1. Yu Yuan & Dawid Jaślan & Taufiq Rahman & Stephen R. Bolsover & Vikas Arige & Larry E. Wagner & Carla Abrahamian & Rachel Tang & Marco Keller & Jonas Hartmann & Anna S. Rosato & Eva-Maria Weiden & Fran, 2022. "Segregated cation flux by TPC2 biases Ca2+ signaling through lysosomes," Nature Communications, Nature, vol. 13(1), pages 1-13, December.

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