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Titolo:
THE ACTIVATION OF ENOS BY COPPER-ION (CU2-CELLS (HPAEC)() IN HUMAN PULMONARY ARTERIAL ENDOTHELIAL)
Autore:
DEMURA Y; AMESHIMA S; ISHIZAKI T; OKAMURA S; MIYAMORI I; MATSUKAWA S;
Indirizzi:
FUKUI MED UNIV,DEPT INTERNAL MED 4,23-3 MATSUOKA CHO FUKUI 91011 JAPAN FUKUI MED UNIV,FAC MED,DEPT INTERNAL MED 3 FUKUI JAPAN FUKUI MED UNIV,FAC MED,CENT RES LABS FUKUI JAPAN
Titolo Testata:
Free radical biology & medicine
fascicolo: 3, volume: 25, anno: 1998,
pagine: 314 - 320
SICI:
0891-5849(1998)25:3<314:TAOEBC>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; EVANS CINNAMON RATS; DIMERIC ENZYME; OXYGEN; METALLOTHIONEIN; SPECTROSCOPY; GLYCATION; DISMUTASE;
Keywords:
COPPER; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; CALCIUM; ENDOTHELIAL CELL; FREE RADICAL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
Y. Demura et al., "THE ACTIVATION OF ENOS BY COPPER-ION (CU2-CELLS (HPAEC)() IN HUMAN PULMONARY ARTERIAL ENDOTHELIAL)", Free radical biology & medicine, 25(3), 1998, pp. 314-320

Abstract

We have previously reported that CU2+ endothelium-dependently dilatedrat pulmonary arterial rings in a few minutes by increasing NO production via constitutive endothelial nitric oxide synthase (eNOS) activation in rat pulmonary arterial endothelial cells (Eur. J. Pharmacol., 1997). In the present study, using cultured human pulmonary arterial endothelial cells (HPAEC), we assessed the effects of divalent cations (Cu2+, Mn2+, Zn2+, and Fe2+) on NOS activity in crude cell extracts andintact cells. NO synthase activity was measured by monitoring the conversion of L-[C-14] arginine to L-[C-14] citrulline. The NOS enzyme incrude HPAEC extract showed similar characteristics to previously reported eNOS from other sources. All the divalent cations tested suppressed the NOS activity in crude cell extract by about 50% at 1 x 10(-4) hi, but only Cu2+ from 10(-6) M increased eNOS activation dose dependently with a significant elevation in whole-cell assay. Extracellular Ca2+ was prerequisite to the eNOS activation by Cu2+ in intact cells. Furthermore, we measured NO production determined as NOx (NO, (NO2-)-N-., and (NO3-)-N-.) from HPAEC using NO chemiluminescence analyzer. HPAEC monolayers were treated with either buffer alone, Cu2+ (10(-4) M) orthapsigargin (10(-6) M). The amount of (. )NOx increased from 10.93 (pmol/ml/10(6) cells) to 41.27 (pmol/ml/10(6) cells) by thapsigargin (10(-6) M) and to 45.24 (pmol/ml/10(6) cells) by Cu2+ (10(-4) M). The increase in NOx by Cu2+ was inhibited by L-NMMA. These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC. Further, our study showed that extracellular Ca2was essential for eNOS activation by Cu2+. (C) 1998 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 10:12:25