Expression of heat shock proteins in the normal and stunned porcine myocardium

Andres, Janusz; Sharma, Hari Shanker; Knöll, Ralph; Stahl, Joachim; Sassen, L. M. A.; Verdouw, Pieter D.; Schäper, Wolfgang

doi:10.1093/cvr/27.8.1421

Cited by 63 publications

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“…The decrease in SR Ca 2÷ uptake rate usually appears after 10-15 min of ischemia [33,34,36]. Such a brief period of ischemia does not lead to irreversible myocardial damage, but upon reperfusion, recovery of contractile function is delayed ("stunned myocardium") [5,7,[41][42][43][44][45]. In the following paragraphs we present some data characterizing the SR Ca 2+ pump function in stunned myocardium.…”

Section: Alterations In the Sr Ca 2 + Pump Function In The Ischemic Amentioning

confidence: 99%

Involvement of the sarcoplasmic reticulum calcium pump in myocardial contractile dysfunction: Comparison between chronic pressure-overload and stunning

Sharma

Verdouw

Lamers

1994

Cardiovasc Drug Ther

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Summary. Acute as well as chronic forms of heart failure involve mechanical dysfunction during systole and/or diastole. The rapid Ca 2+ release from and Ca ~+ reuptake into the tubuli of the sarcoplasmic reticulum are processes that critically determine normal systolic and diastolic myocardial function, which explains why in the last fifteen years so much attention has been paid to understand the performance of the sarcoplasmic reticulum Ca 2+ pump during myocardial contractile dysfunction. In this communication we have reviewed the literature data on sarcoplasmic reticulum Ca 2+ pump function in the chronically pressure-overloaded hypertrophied and stunned (post-ischemic reversibly injured) myocardium in the light of some new data from our laboratory. Results on the pressure-overloaded hypertrophied myocardium provide evidence that impaired relaxation is most likely due to a low capacity of the sarcoplasmic reticulum to pump Ca 2+, a consequence of a lower density of Ca2+-pumping sites within the sarcotubular membranes. Contractile dysfunction in stunned myocardium is accompanied by an upregulation of the sarcoplasmic reticulum Ca ~ + ATPase gene resulting in a slight increase of the Ca2 + pumping activity. The latter increase is likely an adaptive response of the reversibly injured myocardium which may contribute to the slow recovery of contractile function.Cardiovasc Drugs Ther 1994;8:461-468 Key Words. sarcoplasmic reticulum, Ca ~+ pump, hypertrophy, stunning, cardiac failureNormal systolic and diastolic function of the heart requires the release and reuptake of Ca 2+. The contractile state of the heart can be altered by two mechanisms which are both Ca 2+ dependent: changes in the availability of Ca ~÷ to the contractile proteins and changes in the responsiveness of the contractile proteins to activation by intracellular Ca 2+ [1]. The availability of intracellular Ca ~÷ is regulated by the sarcolemma (SL) and sarcoplasmic reticulum (SR) and the Ca 2+ responsiveness is controlled by the myofilaments and regulatory troponin-tropomyosin complex. Excitation-contraction (E-C) coupling is initiated when Ca 2+ channels are opened by depolarization of SL permitting Ca 2+ to enter the cytoplasm. This small Ca 2+ influx induces the release of a much larger quantity of activated Ca 2÷ from the intraeellutar stores in the SR [2,3]. The released Ca 2+ interacts with troponin C, which is part of the regulatory complex of the myofilaments, thereby initiating cardiac contraction. Relaxation starts when Ca 2+ is sequestered by the SR Ca 2+ pump, so that Ca2 ÷ dissociates from the contractile apparatus. Abnormal handling of intracellutar Ca ~+ at any of the steps in E-C coupling can cause cardiae contractile dysfunction and leads to failure. The signalling function of Ca 2+ demands a very low ionic concentration of Ca 2+ inside the myocardial cells (about 10,000 fold lower than outside) and significant changes can therefore be achieved easily. During each depolarization only a very small amount of Ca ~* entering the cell...

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Section: Alterations In the Sr Ca 2 + Pump Function In The Ischemic Amentioning

confidence: 99%

Involvement of the sarcoplasmic reticulum calcium pump in myocardial contractile dysfunction: Comparison between chronic pressure-overload and stunning

Sharma

Verdouw

Lamers

1994

Cardiovasc Drug Ther

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“…Heat shock proteins (HSPs) are a group of highly conserved proteins that can be stimulated by heat shock and other environmental and pathophysiological stresses [23][24][25][26][27][28][29]. Also glucose regulated proteins (GRPs), ubiquitin, c~13-crystalline and heme oxygenase [24][25][26][28][29][30][31][32][33] are included in the group of HSPs.…”

Section: Introductionmentioning

confidence: 99%

“…Also glucose regulated proteins (GRPs), ubiquitin, c~13-crystalline and heme oxygenase [24][25][26][28][29][30][31][32][33] are included in the group of HSPs. These proteins participate in cellular defense mechanisms and enable cells to survive and recover from stressful conditions [23,26,27,34].…”

Section: Introductionmentioning

confidence: 99%

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Cytoprotective mechanisms in cultured cardiomyocytes

Sharma

Stahl

Weisensee

et al. 1996

Biochemical Mechanisms in Heart Function

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Tumor necrosis factor-c~ (TNF-a), a potent cytokine mainly secreted by macrophages exerts pleiotropic effects on different cell types. However, the intracellular mediators of its action are not yet well characterized. To get an insight into endogenous cytoprotective mechanisms, we developed an in vitro model based on cultured cardiomyocytes treated with TNF-c~ at which we examined gene expression of heat shock proteins (HSP-27, HSP-70 and ubiquitin). Cardiomyocytes were isolated from the hearts of 18 day old fetal mice by enzymatic dissociation and grown in minimum essential medium containing 10% fetal calf serum. Spontaneously contractile cells were serum deprived for 24 h and treated with TNF-a (25 ng/ml) for 1, 2, 4, 6, 8, 12, and 24 h After each incubation, cells were processed to extract total proteins for Western and total RNA for Noi"thern blot analyses. TNF-ct induced arrhythmias and cessation of spontaneous contractions in a concentration and time dependent manner. Steady state (ubiquitin) or undetectable mRNA levels (HSP-27, HSP-70) were drastically induced (> 4 fold for all three genes vs untreated control cells) by TNF-c~, reaching maximal values between 6-8 h of stimulation. Thereafter, the expression of these stress genes declined but remained elevated as compared to control. By Western blot analysis, we found increased multiple bands of ubiquitin protein conjugates in TNF-c~ treated cells whereas no significant change in HSP-27 protein accumulation until 12 h was observed as compared to control. 24 h of TNF-ct incubation resulted in partial cellular necrosis. Our results indicate that TNF-c~ induces in cardiomyocytes transiently gene expression for cytoprotective molecules like HSP-27, HSP-70 and ubiquitin, suggesting these stress proteins to participate in subsequent defense mechanisms, for example in postischemic myocardial recovery. (Mol Cell Biochem 160/161:217-224, 1996)

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“…It has been reported that brief periods of ischemia are strong inducers of gene expression. [3][4][5][6] However, a link between increased transcription of a mRNA species and adaptational changes has not been established. 7) In the present study, we employed differential display reverse transcription-polymerase chain reaction (DDRT-PCR) to show the gene expression pattern in rat heart six weeks after MI.…”

mentioning

confidence: 99%

Identification of Regulated Genes in Rat Heart after Myocardial Infarction by Means of Differential mRNA Display.

Zhu

Stoll

et al. 2000

Jpn Heart J

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SUMMARYIn order to testify the hypothesis that unknown mechanisms are involved in the process of cardiac remodeling after myocardial infarction (MI), we employed differential display reverse transcription-polymerase chain reaction (DDRT-PCR) as our primary inspection tool. An animal model of MI was established by ligation of the left anterior descending coronary artery (LAD) in rat. Fifty upregulated candidate cDNA fragments were obtained in the right ventricle (RV) of the heart six weeks after MI. Eight cDNA fragments isolated from DD denaturing gel were extracted and reamplified, cloned into pCR II vector and sequenced. A Genbank search of these clones showed that three of them have a high homology with known genes not previously associated with cardiac remodeling, i.e., mouse interleukin-4 receptor gene, rat ferritin mRNA, and T-cell receptor beta chain V beta 5. The remaining clones have no similarity to known sequences. These data suggest that certain genes which were not previously being associated with cardiac hypertrophy are turned on during the process of cardiac remodeling after MI. (Jpn Heart J 2000; 41: 59-66) Key words: Gene expression, Myocardial infarction, Differential display, Cloning, Polymerase chain reaction M YOCARDIAL infarction (MI) induces remodeling of the viable myocardium and results in cardiac hypertrophy which is an independent cardiovascular risk factor. Numerous studies have been performed to investigate the mechanisms of cardiac hypertrophy, amongst which, activation of the renin angiotensin system (RAS) and endothelin have been demonstrated to be important From the

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Expression of heat shock proteins in the normal and stunned porcine myocardium

Abstract: The findings support the hypothesis that molecular damage occurs in stunned myocardium; however, the target molecules remain to be recognised.

Cited by 63 publications

References 0 publications

Involvement of the sarcoplasmic reticulum calcium pump in myocardial contractile dysfunction: Comparison between chronic pressure-overload and stunning

Involvement of the sarcoplasmic reticulum calcium pump in myocardial contractile dysfunction: Comparison between chronic pressure-overload and stunning

Cytoprotective mechanisms in cultured cardiomyocytes

Identification of Regulated Genes in Rat Heart after Myocardial Infarction by Means of Differential mRNA Display.

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