Nicotinic acid–adenine dinucleotide phosphate (NAADP) elicits specific microsomal Ca2+ release from mammalian cells

2001 ◽  
Vol 353 (3) ◽  
pp. 531-536 ◽  
Author(s):  
Ahad N.-K. YUSUFI ◽  
Jingfei CHENG ◽  
Michael A. THOMPSON ◽  
Eduardo N. CHINI ◽  
Joseph P. GRANDE
Keyword(s):  
Nicotinic Acid ◽  
Intracellular Calcium ◽  
Sea Urchin ◽  
Mammalian Cells ◽  
Calcium Release ◽  
Cultured Cells ◽  
Mesangial Cells ◽  
Rat Kidney ◽  
Leukaemia Cell Line ◽  
Mammalian Tissues

Nicotinic acid–adenine dinucleotide phosphate (NAADP), a molecule derived from β-NADP, has been shown to promote intracellular calcium release in sea urchin eggs. However, there is little information regarding the role of NAADP in the regulation of intracellular calcium fluxes in mammalian cells. We found recently that several mammalian tissues have a high capacity for NAADP synthesis, as assessed by sea urchin egg bioassay. To determine the functional significance of NAADP production by mammalian tissues, we sought to determine whether NAADP is capable of inducing calcium release from microsomes prepared from cultured cells. We found that NAADP, but not β-NADP, activates a specific microsomal calcium release system in mesangial cells isolated from rat kidney; NAADP was without effect in renal tubular epithelial cells. NAADP-induced calcium release is not affected by inhibitors of the inositol 1,4,5-trisphosphate or ryanodine channels. However, NAADP-elicited calcium release was inhibited by L-type calcium channel blockers and by alkaline phosphatase treatment of NAADP. NAADP also promotes specific microsomal calcium release in rat vascular smooth muscle cells, cardiac myocytes, fibroblasts and a human leukaemia cell line, indicating that the capacity for NAADP-induced calcium release is widespread in mammalian cells. We propose that NAADP may be an important regulator of intracellular calcium in many mammalian tissues.

The production of tissue-specific histone complements during development

1988 ◽  
Vol 66 (6) ◽  
pp. 636-649 ◽  
Author(s):  
Ronald W. Lennox ◽  
Leonard H. Cohen
Keyword(s):  
Sea Urchin ◽  
Cultured Cells ◽  
Intact Animal ◽  
Biological Significance ◽  
Tissue Specific ◽  
Major Mechanism ◽  
Mammalian Tissues ◽  
Dividing Cells ◽  
Tissue Differences

At least two mechanisms generate tissue differences in the histone subtype composition during development: subtype dilution and subtype replacement. Subtype dilution, which occurs when cells continue dividing after having ceased to synthesize one or more histone subtypes, allows the elimination of stable subtypes. It is the major mechanism generating cell differences in histone composition in sea urchin embryogenesis. Subtype replacement has been observed in mammalian tissues, both in the intact animal and in cultured cells. It is most evident in nondividing cells but occurs to some extent in dividing cells as well. Examples of the two mechanisms are presented and their possible biological significance, as well as that of the differences they produce, is discussed.

scholarly journals Ca2+ release triggered by NAADP in hepatocyte microsomes

2006 ◽  
Vol 395 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Miklós Mándi ◽  
Balázs Tóth ◽  
György Timár ◽  
Judit Bak
Keyword(s):  
Nicotinic Acid ◽  
Ryanodine Receptor ◽  
Sea Urchin ◽  
Mammalian Cells ◽  
Liver Microsomes ◽  
The Other ◽  
Release Mechanism ◽  
Ip3 Receptors ◽  
Rat Hepatocyte ◽  
Inositol 1,4,5 Trisphosphate

NAADP (nicotinic acid–adenine dinucleotide phosphate) is fast emerging as a new intracellular Ca2+-mobilizing messenger. NAADP induces Ca2+ release by a mechanism that is distinct from IP3 (inositol 1,4,5-trisphosphate)- and cADPR (cADP-ribose)-induced Ca2+ release. In the present study, we demonstrated that micromolar concentrations of NAADP trigger Ca2+ release from rat hepatocyte microsomes. Cross-desensitization to IP3 and cADPR by NAADP did not occur in liver microsomes. We report that non-activating concentrations of NAADP can fully inactivate the NAADP-sensitive Ca2+-release mechanism in hepatocyte microsomes. The ability of thapsigargin to block the NAADP-sensitive Ca2+ release is not observed in sea-urchin eggs or in intact mammalian cells. In contrast with the Ca2+ release induced by IP3 and cADPR, the Ca2+ release induced by NAADP was completely independent of the free extravesicular Ca2+ concentration and pH (in the range 6.4–7.8). The NAADP-elicited Ca2+ release cannot be blocked by the inhibitors of the IP3 receptors and the ryanodine receptor. On the other hand, verapamil and diltiazem do inhibit the NAADP- (but not IP3- or cADPR-) induced Ca2+ release.

Fast calcium wave propagation mediated by electrically conducted excitation and boosted by CICR

2008 ◽  
Vol 294 (4) ◽  
pp. C917-C930 ◽  
Author(s):  
J. M. A. M. Kusters ◽  
W. P. M. van Meerwijk ◽  
D. L. Ypey ◽  
A. P. R. Theuvenet ◽  
C. C. A. M. Gielen
Keyword(s):  
Intracellular Calcium ◽  
Chloride Channels ◽  
Calcium Release ◽  
Rat Kidney ◽  
Electrical Coupling ◽  
Calcium Oscillations ◽  
Calcium Wave ◽  
Calcium Oscillation ◽  
Pacemaker Cell ◽  
Pacemaker Cells

We have investigated synchronization and propagation of calcium oscillations, mediated by gap junctional excitation transmission. For that purpose we used an experimentally based model of normal rat kidney (NRK) cells, electrically coupled in a one-dimensional configuration (linear strand). Fibroblasts such as NRK cells can form an excitable syncytium and generate spontaneous inositol 1,4,5-trisphosphate (IP3)-mediated intracellular calcium waves, which may spread over a monolayer culture in a coordinated fashion. An intracellular calcium oscillation in a pacemaker cell causes a membrane depolarization from within that cell via calcium-activated chloride channels, leading to an L-type calcium channel-based action potential (AP) in that cell. This AP is then transmitted to the electrically connected neighbor cell, and the calcium inflow during that transmitted AP triggers a calcium wave in that neighbor cell by opening of IP3 receptor channels, causing calcium-induced calcium release (CICR). In this way the calcium wave of the pacemaker cell is rapidly propagated by the electrically transmitted AP. Propagation of APs in a strand of cells depends on the number of terminal pacemaker cells, the L-type calcium conductance of the cells, and the electrical coupling between the cells. Our results show that the coupling between IP3-mediated calcium oscillations and AP firing provides a robust mechanism for fast propagation of activity across a network of cells, which is representative for many other cell types such as gastrointestinal cells, urethral cells, and pacemaker cells in the heart.

scholarly journals Nicotinic Acid Adenine Dinucleotide Phosphate: A New Ca2+ Releasing Agent in Kidney

2001 ◽  
Vol 12 (1) ◽  
pp. 54-60 ◽  
Author(s):  
JINGFEI CHENG ◽  
AHAD N. K. YUSUFI ◽  
MICHAEL A. THOMPSON ◽  
EDUARDO N. CHINI ◽  
JOSEPH P. GRANDE
Keyword(s):  
Renal Function ◽  
Retinoic Acid ◽  
Nicotinic Acid ◽  
Hplc Analysis ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Rat Kidney ◽  
Kidney Cortex ◽  
Cyclic Adp Ribose ◽  
Inositol 1,4,5 Trisphosphate

Abstract. Nicotinic acid adenine dinucleotide phosphate (NAADP), a molecule derived from β-NADP, has been shown to trigger Ca2+ release from intracellular stores of invertebrate eggs and mammalian cell microsomes. NAADP-induced Ca2+ release occurs through a mechanism distinct from that of inositol-1,4,5-trisphosphate— or cyclic ADP-ribose—elicited Ca2+ release. This study investigated whether NAADP can be synthesized in rat kidney. Extracts from glomeruli, mesangial cells, and papilla have high NAADP synthetic capacities. Conversely, synthesis of NAADP in kidney cortex was almost undetectable. Furthermore, 9-cis-retinoic acid significantly up-regulated NAADP synthesis in mesangial cells. Authenticity of NAADP biosynthesis in glomeruli was affirmed by HPLC analysis. NAADP stimulated Ca2+ release from mesangial cell microsomes through a pathway distinct from that of inositol-1,4,5-trisphosphate or cyclic ADP-ribose. NAADP-triggered Ca2+ release may play an important role in regulation of renal function.

Modeling action potential generation and propagation in NRK fibroblasts

2004 ◽  
Vol 287 (4) ◽  
pp. C851-C865 ◽  
Author(s):  
J. J. Torres ◽  
L. N. Cornelisse ◽  
E. G. A. Harks ◽  
W. P. M. van Meerwijk ◽  
A. P. R. Theuvenet ◽  
...  
Keyword(s):  
Action Potential ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Cell Transformation ◽  
Rat Kidney ◽  
Potassium Conductance ◽  
Calcium Dynamics ◽  
Starting Point ◽  
Release Analysis ◽  
Intracellular Calcium Dynamics

Normal rat kidney (NRK) fibroblasts change their excitability properties through the various stages of cell proliferation. The present mathematical model has been developed to explain excitability of quiescent (serum deprived) NRK cells. It includes as cell membrane components, on the basis of patch-clamp experiments, an inwardly rectifying potassium conductance ( GKir), an L-type calcium conductance ( GCaL), a leak conductance ( Gleak), an intracellular calcium-activated chloride conductance [ GCl(Ca)], and a gap junctional conductance ( Ggj), coupling neighboring cells in a hexagonal pattern. This membrane model has been extended with simple intracellular calcium dynamics resulting from calcium entry via GCaL channels, intracellular buffering, and calcium extrusion. It reproduces excitability of single NRK cells and cell clusters and intercellular action potential (AP) propagation in NRK cell monolayers. Excitation can be evoked by electrical stimulation, external potassium-induced depolarization, or hormone-induced intracellular calcium release. Analysis shows the roles of the various ion channels in the ultralong (∼30 s) NRK cell AP and reveals the particular role of intracellular calcium dynamics in this AP. We support our earlier conclusion (De Roos A, Willems PH, van Zoelen EJ, and Theuvenet AP. Am J Physiol Cell Physiol 273: C1900–C1907, 1997) that AP generation and propagation may act as a rapid mechanism for the propagation of intracellular calcium waves, thus contributing to fast intercellular calcium signaling. The present model serves as a starting point to further analyze excitability changes during contact inhibition and cell transformation.

scholarly journals Differential regulation of nicotinic acid–adenine dinucleotide phosphate and cADP-ribose production by cAMP and cGMP

1998 ◽  
Vol 331 (3) ◽  
pp. 837-843 ◽  
Author(s):  
Heather L. WILSON ◽  
Antony GALIONE
Keyword(s):  
Nicotinic Acid ◽  
Sea Urchin ◽  
Calcium Release ◽  
Second Messengers ◽  
Differential Regulation ◽  
Sea Urchin Egg ◽  
Inositol 1,4,5 Trisphosphate ◽  
Extracellular Stimuli ◽  
Camp And Cgmp ◽  
Temperature Optima

The sea urchin egg has been used as a system to study calcium-release mechanisms induced by inositol 1,4,5-trisphosphate (IP3), cADP-ribose (cADPR), and more recently, nicotinic acid–adenine dinucleotide phosphate (NAADP). In order that cADPR and NAADP may be established as endogenous messengers for calcium release, the existence of intracellular enzymes capable of metabolizing these molecules must be demonstrated. In addition, intracellular levels of cADPR and NAADP should be under the control of extracellular stimuli. It has been shown that cGMP stimulates the synthesis of cADPR in the sea urchin egg. The present study shows that the sea urchin egg is capable of synthesizing and degrading NAADP. cADPR and NAADP synthetic activities appear to be separate, with different cellular localizations, pH and temperature optima. We suggest that in the sea urchin egg, cADPR and NAADP production may be differentially regulated by receptor-coupled second messengers, with cADPR production being regulated by cGMP and NAADP production modulated by cAMP.

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