Abstract
An intracellular mechanism activated by nicotinic acid adenine dinucleotide phosphate (NAADP(+)) contributes to intracellular Ca(2+) release alongside inositol 1,4,5-trisphosphate (Ins-P(3)) and ryanodine receptors. The NAADP(+)-sensitive mechanism has been shown to be operative in sea urchin eggs, ascidian eggs, and pancreatic acinar cells. Furthermore, most mammalian cell types can synthesize NAADP(+), with nicotinic acid and NADP(+) as precursors. In this contribution, NAADP(+)-induced Ca(2+) release has been investigated in starfish oocytes. Uncaging of injected NAADP(+) induced Ca(2+) mobilization in both immature oocytes and in oocytes matured by the hormone 1-methyladenine (1-MA). The role of extracellular Ca(2+) in NAADP(+)-induced Ca(2+) mobilization, which was minor in immature oocytes, was instead essential in mature oocytes. Thus, the NAADP(+)-sensitive Ca(2+) pool, which is known to be distinct from those sensitive to inositol 1,4,5-trisphosphate or cyclic ADPribose, apparently migrated closer to (or became part of) the plasma membrane during the maturation process. Inhibition of both Ins-P(3) and ryanodine receptors, but not of either alone, substantially inhibited NAADP(+)-induced Ca(2+) mobilization in both immature and mature oocytes. The data also suggest that NAADP(+)-induced Ca(2+) mobilization acted as a trigger for Ca(2+) release via Ins-P(3) and ryanodine receptors.
Highlights
An intracellular mechanism activated by nicotinic acid adenine dinucleotide phosphate (NAADP؉) contributes to intracellular Ca2؉ release alongside inositol 1,4,5-trisphosphate (Ins-P3) and ryanodine receptors
One striking result in this contribution, which deserves to be mentioned at the outset of the “Discussion,” has been the demonstration that the characteristics of the Ca2ϩ-release reaction mediated by NAADPϩ varied with the maturation stage of the cells
The Ca2ϩ spike was sensitive to the simultaneous injection of both heparin and 8-NH2-cADPr, supporting the interplay between the routes activated by Ins-P3/cADPr and that promoted by NAADPϩ
Summary
An intracellular mechanism activated by nicotinic acid adenine dinucleotide phosphate (NAADP؉) contributes to intracellular Ca2؉ release alongside inositol 1,4,5-trisphosphate (Ins-P3) and ryanodine receptors. The NAADP؉sensitive Ca2؉ pool, which is known to be distinct from those sensitive to inositol 1,4,5-trisphosphate or cyclic ADPribose, apparently migrated closer to (or became part of) the plasma membrane during the maturation process Inhibition of both Ins-P3 and ryanodine receptors, but not of either alone, substantially inhibited NAADP؉-induced Ca2؉ mobilization in both immature and mature oocytes. The intracellular Ca2ϩ wave that follows the interaction with the sperm is initiated by Ca2ϩ release via Ins-P31 and ryanodine-sensitive receptors The latter are activated by cADPr [1, 2], an endogenous pyridine. At variance with sea urchins, in ascidians eggs NAADPϩ did not display the low threshold inactivation property In these eggs NAADPϩ blocked the post-fertilization Ca2ϩ oscillations [11], compellingly supporting its physiological role. In line with this suggestion, mammalian cells possess the enzymatic machinery to synthesize and degrade NAADPϩ [12, 13]
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