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Titolo:
On the mechanism of genistein-induced activation of protein kinase A-dependent Cl- conductance in cardiac myocytes
Autore:
Obayashi, K; Horie, M; Washizuka, T; Nishimoto, T; Sasayama, S;
Indirizzi:
Kyoto Univ, Sch Med, Dept Cardiovasc Med, Div Cardiac Electrophysiol,SakyoKu, Kyoto 60601, Japan Kyoto Univ Kyoto Japan 60601 Electrophysiol,SakyoKu, Kyoto 60601, Japan
Titolo Testata:
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
fascicolo: 3, volume: 438, anno: 1999,
pagine: 269 - 277
SICI:
0031-6768(199908)438:3<269:OTMOGA>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
VENTRICULAR MYOCYTES; CHLORIDE CURRENT; INHIBITOR GENISTEIN; MAMMALIAN HEART; CHANNEL BLOCKER; TYROSINE; CFTR; CAMP; PHOSPHORYLATION; ENHANCEMENT;
Keywords:
cardiac CFTR Cl- channel; genistein; protein tyrosine kinase; cAMP-dependent protein kinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Horie, M Kyoto Univ, Sch Med, Dept Cardiovasc Med, Div Cardiac Electrophysiol,SakyoKu, Kyoto 60601, Japan Kyoto Univ Kyoto Japan 60601 hysiol,SakyoKu, Kyoto 60601, Japan
Citazione:
K. Obayashi et al., "On the mechanism of genistein-induced activation of protein kinase A-dependent Cl- conductance in cardiac myocytes", PFLUG ARCH, 438(3), 1999, pp. 269-277

Abstract

Genistein, an inhibitor of protein tyrosine kinase (PTK), enhanced the activation of the cardiac isoform of the protein kinase A (PKA)-regulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-)conductance in guinea-pig ventricular cells. We examined the mechanism(s) underlying this excitatory action of genistein by using patch-clamp techniques. The CFTR Cl- conductance, activated by isoproterenol (ISO, 10 nM; [Cl-] 153 mM extracellular, 21 mM intracellular; 36 degrees C), was enhanced by 20 mu M genistein. Daidzein, a structural analogue of genistein with little inhibitory action on PTK, also enhanced CFTR Cl- currents. After maximal activation of the Cl- conductance by a cocktail of adenosine 3',5'-cyclic monophosphate, 3-isobutyl-1-methylxanthine and okadaic acid or vanadate plus forskolin in the pipette, genistein was no longer stimulatory but was rather slightly inhibitory at 100 mu M. Direct exposure of myocytes to higher concentrations ofgenistein (50-100 mu M) elicited outwardly rectifying currents with a reversal potential of -47 mV in the absence of ISO. In the presence of 50 mu M H-89, a PKA inhibitor, genistein had no effect. Vanadate in the pipette at a concentration (100 CIM) inhibiting phosphotyrosine phosphatases alone didnot prevent the action of genistein. In contrast, no conductance was activated by tyrphostins B42 or 51 or lavendustin A, other PTK inhibitors. Genistein's stimulation of cardiac CFTR Cl- conductance appears to be independent of the PTK pathway and to be due to its direct interaction with CFTR Cl- channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 00:24:06