Identification of the changes in phospholipase C isozymes in ischemic-reperfused rat heart

被引:27
作者
Asemu, G
Tappia, PS [1 ]
Dhalla, NS
机构
[1] Univ Manitoba, Fac Human Ecol & Med, St Boniface Gen Hosp, Inst Cardiovasc Sci,Res Ctr, Winnipeg, MB R2H 2A6, Canada
[2] Univ Manitoba, Fac Human Ecol & Med, Dept Human Nutrit Sci, Winnipeg, MB R2H 2A6, Canada
[3] Univ Manitoba, Fac Human Ecol & Med, Dept Physiol, Winnipeg, MB R2H 2A6, Canada
关键词
phospholipid-mediated signaling pathways; phospholipase C isozymes; heart; sarcolemmal membrane; ischemia-reperfusion; cardiac contractile function;
D O I
10.1016/S0003-9861(02)00733-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Phospholipase C (PLC) influences cardiac function. This study examined PLC isozymes of the cardiac sarcolemma (SL) membrane and in the cytosol compartment in isolated perfused rat hearts subjected to global ischemia for 30 min followed by up to 30 min of reperfusion. Although the total SL PLC activity was decreased in ischemia and increased upon reperfusion, differential changes in PLC isozymes were detected. PLC P, mRNA and SL protein abundance and activity were increased in ischemia, with concomitant decreases in activity and protein level in the cytosol. On the other hand, upon reperfusion, PLC P, activity was decreased, but remained higher than control values. Although no change in the PLC 61 mRNA level in ischemia was detected, SL PLC 61 activity and content were depressed. Furthermore, in the cytosol, PLC 81 activity was increased, but the protein level decreased. SL PLC gamma(1) activity was decreased, independent of gene expression and protein content; however, decreases in the activity and protein abundance were detected in the cytosol. Increases in PLC gamma(1) and delta(1) activities occurred upon reperfusion, but were not accounted for by altered mRNA and protein levels. The results indicate that ischemia-reperfusion induces differential changes in PLC isozymes. (C) 2003 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:174 / 182
页数:9
相关论文
共 49 条
[1]   INOSITOL PHOSPHATE RELEASE AND METABOLISM DURING MYOCARDIAL-ISCHEMIA AND REPERFUSION IN RAT-HEART [J].
ANDERSON, KE ;
DART, AM ;
WOODCOCK, EA .
CIRCULATION RESEARCH, 1995, 76 (02) :261-268
[2]   Phospholipase C-γ1 is required for cell survival in oxidative stress by protein kinase C [J].
Bai, XC ;
Deng, F ;
Liu, AL ;
Zou, ZP ;
Wang, Y ;
Ke, ZY ;
Ji, QS ;
Luo, SQ .
BIOCHEMICAL JOURNAL, 2002, 363 (02) :395-401
[3]   LIMITATIONS OF MYOCARDIAL REVASCULARIZATION IN RESTORATION OF REGIONAL CONTRACTION ABNORMALITIES PRODUCED BY CORONARY-OCCLUSION [J].
BANKA, VS ;
CHADDA, KD ;
HELFANT, RH .
AMERICAN JOURNAL OF CARDIOLOGY, 1974, 34 (02) :164-170
[4]   MYOCARDIAL STUNNING IN MAN [J].
BOLLI, R .
CIRCULATION, 1992, 86 (06) :1671-1691
[5]   A role for delta PKC in cardiac reperfusion injury in vivo [J].
Chen, L ;
Ingaki, K ;
Ikeno, F ;
Lee, F ;
Yock, P ;
Mochly-Rosen, D .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2002, 34 (07) :A38-A38
[6]   Phospholipid signalling in the nucleus [J].
D'Santos, CS ;
Clarke, JH ;
Divecha, N .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS, 1998, 1436 (1-2) :201-232
[7]   Gene expression after short periods of coronary occlusion [J].
Deindl, E ;
Schaper, W .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 1998, 186 (1-2) :43-51
[8]  
Dhalla NS, 1999, CAN J CARDIOL, V15, P587
[9]  
DHALLA NS, 2000, HEART PHYSL PATHOPHY, P949
[10]  
DHALLA NS, 2002, EMERGING THERAPEUTIC, V5, P205