Heat shock protein expression in hearts hypertrophied by genetic and nongenetic hypertension

被引:5
作者
Iwabuchi, K [1 ]
Tajima, M [1 ]
Isoyama, S [1 ]
机构
[1] Tohoku Univ, Sch Med, Dept Internal Med 1, Aoba Ku, Sendai, Miyagi 9808574, Japan
关键词
HSP72; HSP; 73; rat; c-jun; c-fos; mRNA; coronary occlusion; heat;
D O I
10.1007/BF02750641
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Genetically hypertensive animals are characterized by greater thermosensitivity and overexpression of heat shock proteins (HSP) upon thermal stimulation. We examined HSP72 expression under conditions of brief coronary occlusion or thermal stimulation,, and the effects of the severity of these stimuli and of myocardial hypertrophy on the expression in hearts of spontaneously hypertensive rat (SHR) and Wistar Kyoto rat (WKY) groups, A snare was created around the left coronary artery in the SHR (n = 16) and WKY (n = 19) groups. In 7 WKY rats, the ascending aorta was banded and a snare was created simultaneously (WKY-AoB). By tying the snare, 4 weeks later, we applied 5- or 10-min coronary occlusion without opening the chest. For thermal stimulation, the SHR (n = 13) and WKY (n = 11) rats were placed in a 42 degrees C chamber for 15 or 40 min. The mRNA or protein level was estimated 1 or 24h after stimulation. In the SHR vs WKY groups, the mRNA and protein levels were higher after 5-min occlusion or 15-min thermal stimulation. After 10-min occlusion or 40-min thermal stimulation the difference was no longer observed. The overexpression was not observed in the WKY-AoB group despite the presence of hypertrophy similar to that seen in the SHR group (3.11 +/- 0.11 vs 3.20 +/- 0.06mg/g in left ventricular weight/body weight). The HSP72 was overexpressed in hearts of genetically hypertensive animals after brief ischemia. Differential expression between the two groups was observed after mild stimuli, but not after more severe stimuli. Cardiac hypertrophy was not a major factor for determining the overexpression of HSP72.
引用
收藏
页码:30 / 39
页数:10
相关论文
共 31 条
[1]   HYPERTENSION, AGING, AND MYOCARDIAL SYNTHESIS OF HEAT-SHOCK PROTEIN-72 [J].
BONGRAZIO, M ;
COMINI, L ;
GAIA, G ;
BACHETTI, T ;
FERRARI, R .
HYPERTENSION, 1994, 24 (05) :620-624
[2]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[3]   HEAT-SHOCK PROTEIN INDUCTION IN RAT HEARTS - A ROLE FOR IMPROVED MYOCARDIAL SALVAGE AFTER ISCHEMIA AND REPERFUSION [J].
DONNELLY, TJ ;
SIEVERS, RE ;
VISSERN, FLJ ;
WELCH, WJ ;
WOLFE, CL .
CIRCULATION, 1992, 85 (02) :769-778
[4]  
Hamet P, 1996, HYPERTENSION, V28, P1112
[5]  
HAMET P, 1990, J HYPERTENS, V8, pS47
[6]   INCREASED TRANSCRIPTION OF A MAJOR STRESS GENE IN SPONTANEOUSLY HYPERTENSIVE MICE [J].
HAMET, P ;
MALO, D ;
TREMBLAY, J .
HYPERTENSION, 1990, 15 (06) :904-908
[7]  
HARRIS EL, 1995, J HYPERTENS, V13, P397
[8]  
HASHIMOTO T, 1991, J HYPERTENS, V9, pS170
[9]   HEAT-SHOCK PROTEIN INDUCTION IN RAT HEARTS - A DIRECT CORRELATION BETWEEN THE AMOUNT OF HEAT-SHOCK PROTEIN-INDUCED AND THE DEGREE OF MYOCARDIAL PROTECTION [J].
HUTTER, MM ;
SIEVERS, RE ;
BARBOSA, V ;
WOLFE, CL .
CIRCULATION, 1994, 89 (01) :355-360
[10]   INDIRECT SYSTOLIC AND MEAN BLOOD-PRESSURE DETERMINATION BY A NEW TAIL CUFF METHOD IN SPONTANEOUSLY HYPERTENSIVE RATS [J].
IKEDA, K ;
NARA, Y ;
YAMORI, Y .
LABORATORY ANIMALS, 1991, 25 (01) :26-29