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Titolo:
Role of protein kinase C and phosphatases in the pulmonary vasculature of neonatal piglets
Autore:
Berkenbosch, JW; Baribeau, J; Ferretti, E; Perreault, T;
Indirizzi:
Univ Missouri, Hlth Sci Ctr, Dept Child Hlth, Div Pediat Crit Care, Columbia, MO 65201 USA Univ Missouri Columbia MO USA 65201 iat Crit Care, Columbia, MO 65201 USA McGill Univ, Montreal Childrens Hosp, Div Newborn Med, Montreal, PQ H3H 1P3, Canada McGill Univ Montreal PQ Canada H3H 1P3 Med, Montreal, PQ H3H 1P3, Canada McGill Univ, Montreal Childrens Hosp, Dept Pediat, Montreal, PQ H3H 1P3, Canada McGill Univ Montreal PQ Canada H3H 1P3 diat, Montreal, PQ H3H 1P3, Canada CUSE Fleurimont, Dept Neonatol, Sherbrooke, PQ, Canada CUSE Fleurimont Sherbrooke PQ Canada pt Neonatol, Sherbrooke, PQ, Canada
Titolo Testata:
CRITICAL CARE MEDICINE
fascicolo: 6, volume: 29, anno: 2001,
pagine: 1229 - 1233
SICI:
0090-3493(200106)29:6<1229:ROPKCA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE CELLS; TYROSINE PHOSPHATASES; SIGNAL-TRANSDUCTION; HYPERTENSION; ENDOTHELIN; VASOCONSTRICTION; DIACYLGLYCEROL; CIRCULATION; MECHANISM; RECEPTOR;
Keywords:
1-oleyl-2-acetyl-glycerol; phorbol 12,13-dibutyrate; chelerythrine; genistein; nifedipine; phenylarsine oxide; staurosporine; isolated perfused lung;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Berkenbosch, JW Univ Missouri, Hlth Sci Ctr, Dept Child Hlth, Div Pediat Crit Care, Columbia, MO 65201 USA Univ Missouri Columbia MO USA 65201 olumbia, MO 65201 USA
Citazione:
J.W. Berkenbosch et al., "Role of protein kinase C and phosphatases in the pulmonary vasculature of neonatal piglets", CRIT CARE M, 29(6), 2001, pp. 1229-1233

Abstract

Objective: Persistent pulmonary hypertension of the newborn is characterized by the presence of intense vasoconstriction and vascular remodeling. Protein tyrosine phosphorylation has been recognized as a critical regulatory element in signal transduction, because it is dynamically regulated by the opposing actions of protein tyrosine kinases and protein tyrosine phosphatases. The objectives of this study were to investigate the role of protein kinase G and phosphatases in the neonatal pulmonary vasculature of normoxic and chronically hypoxic piglets. Design: Prospective, randomized, unblinded study. Setting: Hospital research laboratory. Subjects: Newborn Yorkshire-Landrace piglets. Interventions: Normoxic animals were 3-6 days old. Hypoxic animals were exposed to hypoxia (Flo(2) 0.10) between 1 and 15 days of age to induce pulmonary hypertension and then were studied. Measurements and Main Results: In isolated perfused lungs from normoxic piglets, we measured the perfusion pressure to assess the vasoconstrictor response to protein kinase G activation with phorbol 12,13-dibutyrate or 1-oleyl-2-acetyl-glycerol. We also assessed the effect of protein kinase C inhibition with staurosporine (2 x 10(-6)M) and chelerythrine (5 x 10(-5)M) on endothelin-1-induced pulmonary vasoconstriction. We then examined the effectof chelerythrine and phosphatase inhibition with phenylarsine oxide on thebaseline perfusion pressure of normoxic and chronically hypoxic piglets. Phorbol 12,13-dibutyrate and 1-oleyl-2-acetyl-glycerol caused a sustained, dose-dependent increase in perfusion pressure, with relative potencies about100- and 1000-fold less than endothelin-1, respectively. Protein kinase G inhibitors, chelerythrine and staurosporine, decreased the constrictor response to endothelin-1. Chelerythrine did not affect baseline perfusion pressure in the normoxic animal, whereas it lowered pulmonary vascular tone in chronically hypoxic animals. With respect to phosphatases, phenylarsine oxide significantly increased perfusion pressure in normoxia as well as in hypoxia. Conclusions: These findings confirm that protein kinase C activation causes sustained vasoconstriction in the neonatal pulmonary vasculature and mediates the vasoconstrictor action of potent peptides, like endothelin-1. These findings also confirm that protein kinase C activation could be induced by hypoxic exposure in the neonatal piglet pulmonary vasculature. Phosphatases appear to modulate pulmonary vascular tone in the normoxic and hypoxic newborn piglet.

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Documento generato il 29/03/20 alle ore 18:22:10