Chini E N, Dousa T P
Department of Physiology, Biophysics and Internal Medicine, Mayo Clinic and Foundation, Rochester MN 55905, USA.
Biochem J. 1996 Jun 15;316 ( Pt 3)(Pt 3):709-11. doi: 10.1042/bj3160709.
We investigated the dependence of nicotinate-adenine dinucleotide phosphate (NAADP)-induced Ca2+ release from intracellular stores of sea urchin egg homogenates, upon extravesicular Ca2+. In contrast to the Ca2+ release induced inositol 1',4',5'-triphosphate (IP3) or cyclic ADP-ribose (cADPR), the Ca2+ release induced by NAADP was completely independent of the free extravesicular Ca2+ over a wide range of concentrations (0-0.1 mM). The Ca2+ release triggered by either cADPR or IP3 was biphasically modulated by extravesicular Ca2+, and the Ca2+ release by these agents was abolished when the extravesicular Ca2+ was removed by chelation with 2 mM EGTA. On the other hand, NAADP-triggered Ca2+ release was not influenced by EGTA. These data indicate that while both cADPR and IP3 systems behave as functional Ca(2+)-induced Ca2+ release mechanisms, NAADP activates a Ca2+ release mechanism which is independent of the presence of extravesicular Ca2+. Therefore, the NAADP-sensitive Ca2+ release mechanisms may have a unique regulatory impact upon intracellular Ca2+ homoeostasis.
我们研究了烟酰胺腺嘌呤二核苷酸磷酸（NAADP）诱导的海胆卵匀浆细胞内储存库中Ca2+释放对细胞外Ca2+的依赖性。与肌醇1',4',5'-三磷酸（IP3）或环ADP核糖（cADPR）诱导的Ca2+释放不同，NAADP诱导的Ca2+释放在很宽的浓度范围（0 - 0.1 mM）内完全独立于细胞外游离Ca2+。cADPR或IP3触发的Ca2+释放受到细胞外Ca2+的双相调节，当用2 mM乙二醇双（2-氨基乙醚）四乙酸（EGTA）螯合去除细胞外Ca2+时，这些试剂诱导的Ca2+释放被消除。另一方面，NAADP触发的Ca2+释放不受EGTA影响。这些数据表明，虽然cADPR和IP3系统都表现为功能性的Ca(2+)诱导的Ca2+释放机制，但NAADP激活了一种独立于细胞外Ca2+存在的Ca2+释放机制。因此，对NAADP敏感的Ca2+释放机制可能对细胞内Ca2+稳态具有独特的调节作用。
