Sarcoplasmic reticulum gene expression in post-ischemic congestive heart failure

1992 ◽  
Vol 24 ◽  
pp. 67
Author(s):  
Nasir Afzal ◽  
Angel Zarain-Herzberg ◽  
Naranjan S Dhalla
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Ischemic Congestive Heart Failure

Skeletal Muscle Sarcoplasmic Reticulum Ca 2+ -ATPase Gene Expression in Congestive Heart Failure

1997 ◽  
Vol 81 (5) ◽  
pp. 703-710 ◽  
Author(s):  
David G. Peters ◽  
Heather L. Mitchell ◽  
Sylvia A. McCune ◽  
Sonhee Park ◽  
Jay H. Williams ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Atpase Gene

Influence of long-term treatment of imidapril on mortality, cardiac function, and gene expression in congestive heart failure due to myocardial infarction

2004 ◽  
Vol 82 (12) ◽  
pp. 1118-1127 ◽  
Author(s):  
Bin Ren ◽  
Qiming Shao ◽  
Pallab K Ganguly ◽  
Paramjit S Tappia ◽  
Nobuakira Takeda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Function ◽  
Term Treatment ◽  
Cardiac Performance ◽  
Long Term Treatment

Although it is generally accepted that the efficacy of imidapril, an angiotensin-converting enzyme inhibitor, in congestive heart failure (CHF) is due to improvement of hemodynamic parameters, the significance of its effect on gene expression for sarcolemma (SL) and sarcoplasmic reticulum (SR) proteins has not been fully understood. In this study, we examined the effects of long-term treatment of imidapril on mortality, cardiac function, and gene expression for SL Na+/K+ ATPase and Na+–Ca2+ exchanger as well as SR Ca2+ pump ATPase, Ca2+ release channel (ryanodine receptor), phospholamban, and calsequestrin in CHF due to myocardial infarction. Heart failure subsequent to myocardial infarction was induced by occluding the left coronary artery in rats, and treatment with imidapril (1 mg·kg–1·day–1) was started orally at the end of 3 weeks after surgery and continued for 37 weeks. The animals were assessed hemody nam ically and the heart and lung were examined morphologically. Some hearts were immediately frozen at –70 °C for the isolation of RNA as well as SL and SR membranes. The mortality of imidapril-treated animals due to heart failure was 31% whereas that of the untreated heart failure group was 64%. Imidapril treatment improved cardiac performance, attenuated cardiac remodeling, and reduced morphological changes in the heart and lung. The depressed SL Na+/K+ ATPase and increased SL Na+–Ca2+ exchange activities as well as reduced SR Ca2+ pump and SR Ca2+ release activities in the failing hearts were partially prevented by imidapril. Although changes in gene expression for SL Na+/K+ ATPase isoforms as well as Na+–Ca2+ exchanger and SR phospholamban were attenuated by treatments with imidapril, no alterations in mRNA levels for SR Ca2+ pump proteins and Ca2+ release channels were seen in the untreated or treated rats with heart failure. These results suggest that the beneficial effects of imidapril in CHF may be due to improvements in cardiac performance and changes in SL gene expression.Key words: sarcolemmal Na+/K+ ATPase, Na+–Ca2+ exchange, sarcoplasmic reticulum, heart failure, ACE inhibition.

Myocardial calcium cycling defect in furazolidone cardiomyopathy

1991 ◽  
Vol 69 (12) ◽  
pp. 1833-1840 ◽  
Author(s):  
Peter James O'Brien ◽  
Hua Shen ◽  
Janice E. Weiler ◽  
S. Mehdi Mirsalimi ◽  
Richard J. Julian
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Ruthenium Red ◽  
Channel Activity ◽  
Release Channel ◽  
Calcium Sequestration ◽  
Pump Activity ◽  
Highly Correlated ◽  
Sarcoplasmic Reticulum Calcium

We have previously demonstrated that in furazolidone-induced congestive heart failure in turkeys the specific Ca2+-ATPase activity of myocardial sarcoplasmic reticulum (SR) is 60% increased in compensation for a 50% depression in net Ca2+-sequestration activity. This study tested the hypothesis that SR Ca2+-uptake and Ca2+-ATPase activities were uncoupled in this cardiomyopathy because of increased Ca2+-release channel activity. A novel microassay was used to monitor Ca2+ transport by myocardial homogenates using the fluorescent Ca2+ dye indo 1 to indicate extravesicular ionized Ca2+. The method is applied to cyropreserved biopsy specimens of myocardium and requires only 50 mg tissue. Both SR Ca2+-pump and SR Ca2+-channel activity were estimated using the channel-inhibitor ruthenium red (RR) and the mitochondrial inhibitor sodium azide. The specificity of the RR inhibition was confirmed using ryanodine. Cardiomyopathy was induced in 2-week-old turkey pouits by the addition of 0.07% furazolidone to their feed for 4 weeks. Compared with controls, myocardial maximal Ca2+-channel activity relative to maximal Ca2+-pump activity was 22% greater and duration of Ca2+-channel activity was 100% increased. However, the heart failure birds had 43 and 53% decreases in absolute maximal Ca2+-pumping and Ca2+-channel activities, respectively. The abnormal Ca2+-channel activity resulted in 200% greater time before initiation of net Ca2+ sequestration and 700% greater final myocardial Ca2+ concentrations. For all birds, the Ca2+-accumulating activity was highly correlated with Ca2+-release activity (all p < 0.05). These data indicate that in this animal model of congestive heart failure there is defective SR Ca2+-channel function resulting in abnormal Ca2+ homeostasis. However, this defect can only partially explain our previous finding of furazolidone-induced uncoupling of Ca2+ uptake from Ca2+-ATPase activities. The consequent myocardial Ca2+ overload predisposes the heart to fatigue and irreversible failure.Key words: sarcoplasmic reticulum, calcium sequestration, furazolidone cardiomyopathy, indo 1 spectrofluorometry.

Myocardial Gene Expression of Regulators of Myocyte Apoptosis and Myocyte Calcium Homeostasis During Hemodynamic Unloading by Ventricular Assist Devices in Patients With End-Stage Heart Failure

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Babett Bartling ◽  
Hendrik Milting ◽  
Heike Schumann ◽  
Dorothea Darmer ◽  
Lativ Arusoglu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Sarcoplasmic Reticulum ◽  
Calcium Homeostasis ◽  
Cardiac Transplantation ◽  
Left Ventricular ◽  
Ventricular Assist ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Myocardial Gene Expression

Background —In patients with end-stage heart failure, characterized by an increased susceptibility to cardiomyocyte apoptosis and a labile cardiomyocyte calcium homeostasis, a ventricular assist device (VAD) is implanted for bridging to cardiac transplantation and results in myocardial unloading. Although phenotype changes in the failing heart are assumed to result from hemodynamic overload, the reversibility of these changes under unloading is unknown. Methods and Results —By use of quantitative reverse-transcription polymerase chain reaction, mRNA expression analyses were performed on left ventricular specimens obtained from 10 nonfailing donor hearts (from 8 patients with dilated cardiomyopathy and 2 patients with coronary heart disease) at the time of VAD implantation and 36 to 169 days later during VAD removal with subsequent cardiac transplantation. In terminally failing hearts before VAD support, left ventricular mRNA analyses revealed increased Pro-ANP, reduced antiapoptotic Bcl-x L and antiapoptotic Fas isoform FasExo6Del, and a decreased ratio of sarcoplasmic reticulum Ca 2+ -ATPase per sarcolemmal Na + -Ca 2+ exchanger in comparison with nonfailing ventricles. After VAD unloading, ventricular transcription of Pro-ANP was immediately normalized, and apoptotic DNA fragmentation was attenuated. In patients with dilated cardiomyopathy, mRNAs of Bcl-x L and FasExo6Del/Fas were enhanced depending on time on VAD. The Bcl-x L mRNA level correlated positively with that of the Bcl-x L protein. Transcription of sarcoplasmic reticulum Ca 2+ -ATPase/Na + -Ca 2+ exchanger demonstrated recovery in only 4 of 10 patients. Conclusions —Mechanical support of the failing heart induces a time-dependent change in myocardial gene expression compatible with a decreased susceptibility to apoptosis.

Sign in / Sign up

Export Citation Format

Share Document