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J. Biol. Chem., Vol. 281, Issue 23, 15923-15928, June 9, 2006

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Messenger-specific Role for Nicotinic Acid Adenine Dinucleotide Phosphate in Neuronal Differentiation^*

Eugen Brailoiu, Dev Churamani, Vinita Pandey, G. Cristina Brailoiu, Florin Tuluc, Sandip Patel¹, and Nae J. Dun

From the Department of Pharmacology, Temple University Medical School, Philadelphia, Pennsylvania and the Department of Physiology, University College London, London WC1E 6BT, United Kingdom

Cells possess several Ca²⁺-mobilizing messengers, which couple stimulation at the cell surface by a multitude of extracellular cues to the regulation of intracellular Ca²⁺-sensitive targets. Recent studies suggest that agonists differentially select from this molecular palette to generate their characteristic Ca²⁺ signals but it is still unclear whether different messengers mediate different functions or whether they act in a redundant fashion. In this study, we compared the effects of nicotinic acid adenine dinucleotide phosphate (NAADP), a novel Ca²⁺-mobilizing messenger, with that of the prototypical messenger inositol trisphosphate on cytosolic Ca²⁺ levels and differentiation status of PC12 cells. We demonstrate that liposomal delivery of NAADP mediated release of Ca²⁺ from acidic Ca²⁺ stores and that this stimulus was sufficient to drive differentiation of the cells to a neuronal-like phenotype. In sharp contrast, cell fate was unaffected by more transient Ca²⁺ signals generated by inositol trisphosphate-evoked release of endoplasmic reticulum Ca²⁺ stores. Our data establish for the first time (i) the presence of novel NAADP-sensitive Ca²⁺ stores in PC12 cells, (ii) a role for NAADP in differentiation, and (iii) that Ca²⁺-dependent function can be messenger-specific. Thus, differential recruitment of intracellular Ca²⁺-mobilizing messengers and their target Ca²⁺ stores may represent a robust means of maintaining stimulus fidelity in the control of Ca²⁺-dependent cell function.

Received for publication, March 9, 2006 , and in revised form, March 24, 2006.

^* This work was supported by grants from the National Institutes of Health (to N. J. D.) and the Wellcome Trust, UK (to S. P.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: The Old Squash Courts, Dept. of Physiology, University College London, Gower St., London WC1E 6BT, UK. Tel.: 44-207-679-6540; Fax: 44-207-813-0530; E-mail: patel.s{at}ucl.ac.uk.

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