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Nicotinic Acid Adenine Dinucleotide Phosphate
Author(s) -
Jingfei Cheng,
Ahad N.K. Yusufi,
Michael A. Thompson,
Eduardo N. Chini,
Joseph P. Grande
Publication year - 2001
Publication title -
journal of the american society of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.451
H-Index - 279
eISSN - 1533-3450
pISSN - 1046-6673
DOI - 10.1681/asn.v12154
Subject(s) - biochemistry , inositol , inositol trisphosphate , intracellular , microsome , chemistry , nicotinamide adenine dinucleotide phosphate , inositol phosphate , mesangial cell , nicotinic agonist , biology , receptor , in vitro , enzyme , oxidase test
. Nicotinic acid adenine dinucleotide phosphate (NAADP), a molecule derived from β-NADP, has been shown to trigger Ca 2+ release from intracellular stores of invertebrate eggs and mammalian cell microsomes. NAADP-induced Ca 2+ release occurs through a mechanism distinct from that of inositol-1,4,5-trisphosphate— or cyclic ADP-ribose—elicited Ca 2+ 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 Ca 2+ release from mesangial cell microsomes through a pathway distinct from that of inositol-1,4,5-trisphosphate or cyclic ADP-ribose. NAADP-triggered Ca 2+ release may play an important role in regulation of renal function.

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