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

A. N K Yusufi, J. Cheng, M. A. Thompson, Eduardo Nunes Chini, Joseph Peter Grande

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)531-536
Number of pages6
JournalBiochemical Journal
Volume353
Issue number3
DOIs
StatePublished - Feb 1 2001

Fingerprint

Cells
Calcium
Sea Urchins
Tissue
NADP
NAADP
Rats
Kidney
Ryanodine
L-Type Calcium Channels
Inositol 1,4,5-Trisphosphate
Mesangial Cells
Bioassay
Calcium Channel Blockers
Fibroblasts
Microsomes
Vascular Smooth Muscle
Cardiac Myocytes
Biological Assay
Eggs

Keywords

  • Calcium
  • Cyclic ADP-ribose
  • Inositol trisphosphate
  • Mesangial cells
  • Ryanodine

ASJC Scopus subject areas

  • Biochemistry

Cite this

Nicotinic acid-adenine dinucleotide phosphate (NAADP) elicits specific microsomal Ca2+ release from mammalian cells. / Yusufi, A. N K; Cheng, J.; Thompson, M. A.; Chini, Eduardo Nunes; Grande, Joseph Peter.

In: Biochemical Journal, Vol. 353, No. 3, 01.02.2001, p. 531-536.

Research output: Contribution to journalArticle

@article{a93f7fb2eeb8492ea0185706b8d5bb29,
title = "Nicotinic acid-adenine dinucleotide phosphate (NAADP) elicits specific microsomal Ca2+ release from mammalian cells",
abstract = "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.",
keywords = "Calcium, Cyclic ADP-ribose, Inositol trisphosphate, Mesangial cells, Ryanodine",
author = "Yusufi, {A. N K} and J. Cheng and Thompson, {M. A.} and Chini, {Eduardo Nunes} and Grande, {Joseph Peter}",
year = "2001",
month = "2",
day = "1",
doi = "10.1042/0264-6021:3530531",
language = "English (US)",
volume = "353",
pages = "531--536",
journal = "Biochemical Journal",
issn = "0264-6021",
publisher = "Portland Press Ltd.",
number = "3",

}

TY - JOUR

T1 - Nicotinic acid-adenine dinucleotide phosphate (NAADP) elicits specific microsomal Ca2+ release from mammalian cells

AU - Yusufi, A. N K

AU - Cheng, J.

AU - Thompson, M. A.

AU - Chini, Eduardo Nunes

AU - Grande, Joseph Peter

PY - 2001/2/1

Y1 - 2001/2/1

N2 - 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.

AB - 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.

KW - Calcium

KW - Cyclic ADP-ribose

KW - Inositol trisphosphate

KW - Mesangial cells

KW - Ryanodine

UR - http://www.scopus.com/inward/record.url?scp=0035253080&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035253080&partnerID=8YFLogxK

U2 - 10.1042/0264-6021:3530531

DO - 10.1042/0264-6021:3530531

M3 - Article

C2 - 11171049

AN - SCOPUS:0035253080

VL - 353

SP - 531

EP - 536

JO - Biochemical Journal

JF - Biochemical Journal

SN - 0264-6021

IS - 3

ER -