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Titolo:
The small G-protein Rac mediates depolarization-induced superoxide formation in human endothelial cells
Autore:
Sohn, HY; Keller, M; Gloe, T; Morawietz, H; Rueckschloss, U; Pohl, U;
Indirizzi:
Univ Munich, Inst Physiol, D-80336 Munich, Germany Univ Munich Munich Germany D-80336 Inst Physiol, D-80336 Munich, Germany Univ Halle, Inst Pathophysiol, D-06097 Halle, Germany Univ Halle Halle Germany D-06097 st Pathophysiol, D-06097 Halle, Germany
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 25, volume: 275, anno: 2000,
pagine: 18745 - 18750
SICI:
0021-9258(20000623)275:25<18745:TSGRMD>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY BURST OXIDASE; SMOOTH-MUSCLE CELLS; MEMBRANE-POTENTIAL CHANGES; MESSENGER-RNA EXPRESSION; NADPH OXIDASE; TYROSINE PHOSPHORYLATION; HUMAN-NEUTROPHILS; KINASE-C; HYPERTENSIVE RATS; HYDROGEN-PEROXIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Sohn, HY Univ Munich, Inst Physiol, Schillerstr 44, D-80336 Munich, Germany Univ Munich Schillerstr 44 Munich Germany D-80336 unich, Germany
Citazione:
H.Y. Sohn et al., "The small G-protein Rac mediates depolarization-induced superoxide formation in human endothelial cells", J BIOL CHEM, 275(25), 2000, pp. 18745-18750

Abstract

Superoxide anions impair nitric oxide-mediated responses and are involved in the development of hypertensive vascular hypertrophy, The regulation of their production in the vascular system is, however, poorly understood. We investigated whether changes in membrane potential that occur in hypertensive vessels modulate endothelial superoxide production, In cultured human umbilical vein endothelial cells, changes in membrane potential were induced by high potassium buffer, the non-selective potassium channel blocker tetrabutylammonium chloride (1 mM), and the non-selective cat ion ionophore gramicidin (1 mu M). Superoxide formation was significantly elevated to a similar degree by all three treatments (by similar to 60%, n = 23, p < 0.01), whereas hyperpolarization by the K-ATP channel activator Hoe234 (1 mu M) significantly decreased superoxide formation. Depolarization also induced an increased tyrosine phosphorylation of several not yet identified proteins (90-110 kDa) and resulted in a significant increase in membrane association ofthe small G-protein Rac. Accordingly, the Rac inhibitor Clostridium difficile toxin B blocked the effects of depolarization on superoxide formation. The tyrosine kinase inhibitor genistein (30 mu M, n = 15) abolished depolarization-induced superoxide formation and also prevented depolarization-induced Rac translocation associated with it. It is concluded that depolarization is an important stimulus of endothelial superoxide production, which involves a tyrosine phosphorylation-dependent translocation of the small G-protein Rac.

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Documento generato il 10/07/20 alle ore 12:50:25