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Titolo:
IDENTIFICATION OF CHANGES IN CARDIAC PHOSPHOLIPASE-C ACTIVITY IN CONGESTIVE-HEART-FAILURE
Autore:
MEIJ JTA; PANAGIA V; MESAELI N; PEACHELL JL; AFZAL N; DHALLA NS;
Indirizzi:
ST BONIFACE GEN HOSP,RES CTR,LAB MEMBRANE BIOL,INST CARDIOVASC SCI,351 TACHE AVE WINNIPEG MB R2H 2A6 CANADA ST BONIFACE GEN HOSP,RES CTR,LAB MEMBRANE BIOL,INST CARDIOVASC SCI WINNIPEG MB R2H 2A6 CANADA UNIV MANITOBA,FAC MED,DEPT PHYSIOL WINNIPEG MB R2H 2A6 CANADA UNIV MANITOBA,FAC MED,DEPT ANAT WINNIPEG MB R2H 2A6 CANADA
Titolo Testata:
Journal of Molecular and Cellular Cardiology
fascicolo: 1, volume: 29, anno: 1997,
pagine: 237 - 246
SICI:
0022-2828(1997)29:1<237:IOCICP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR FAILURE; MYOCARDIAL-INFARCTION; INOSITOL TRISPHOSPHATE; PHOSPHATIDYLINOSITOL CYCLE; SARCOPLASMIC-RETICULUM; RAT CARDIOMYOCYTES; CALCIUM-TRANSPORT; FREE-RADICALS; SARCOLEMMA; MYOCYTES;
Keywords:
POST-INFARCTED FAILING HEART; SARCOLEMMAL PHOSPHOLIPASE C; CYTOSOLIC PHOSPHOLIPASE C; PHOSPHATIDYLINOSITOL POLYPHOSPHATES HYDROLYSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
J.T.A. Meij et al., "IDENTIFICATION OF CHANGES IN CARDIAC PHOSPHOLIPASE-C ACTIVITY IN CONGESTIVE-HEART-FAILURE", Journal of Molecular and Cellular Cardiology, 29(1), 1997, pp. 237-246

Abstract

Although phosphoinositide-specific phospholipase C (PLC) is involved in signal transduction mechanisms of the myocardial cell, very little is known about its status in congestive heart failure (CHF). We have examined the PLC activity in sarcolemmal and cytosolic fractions isolated from the viable left ventricle of rats at 8 weeks (moderate stage of CHF) and 16 weeks (severe stage of CHF) after occlusion of the left anterior descending coronary artery; the hypertrophied right ventriclewas used for comparison. At 8 weeks, the hydrolysis of phosphatidylinositol 4,5-bisphosphate by sarcolemmal PLC was reduced by 37% of sham control values only in the left ventricle, whereas at 16 weeks, PLC-mediated hydrolysis was depressed in both left and right ventricles by 25% and 30%, respectively. The hydrolysis of phosphatidylinositol 4-monophosphate (PIP) was reduced by 25% of control value only in the severely failing left ventricle, while the phosphatidylinositol (PI) hydrolysis remained unaltered. Kinetic studies of PLC activity in the left ventricle showed a depression of V-max at moderate and severe failure stages, whereas the affinity for the substrate was increased in the left ventricle at 8 weeks and decreased in the right ventricle at 16 weeks. The only difference observed between experimental and control groups at the cytosolic level, was a significant enhancement of PLC activity in the severely failing left ventricle when PIP was given as a substrate, and in the corresponding right ventricle when PI was the substrate. The results of this study identify time-related defects in sarcolemmal PLC in right and left ventricles during the development of CHF due to myocardial infarction. (C) 1997 Academic Press Limited.

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Documento generato il 03/12/20 alle ore 15:16:56