Unaltered ryanodine receptor protein levels in ischemic cardiomyopathy
| Autor: | Wolfgang Schillinger, Gerd Hasenfuss, Hanjörg Just, Katsuhiko Mikoshiba, Goro Kuwajima, Markus Meyer |
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| Rok vydání: | 1996 |
| Předmět: |
Adult
Male medicine.medical_specialty Clinical Biochemistry Sarcoplasm Blotting Western Myocardial Ischemia Muscle Proteins Calcium-Transporting ATPases Calsequestrin Ryanodine receptor 2 Internal medicine medicine Humans RNA Messenger Molecular Biology Ischemic cardiomyopathy Chemistry Ryanodine receptor Endoplasmic reticulum Myocardium Dilated cardiomyopathy Ryanodine Receptor Calcium Release Channel Cell Biology General Medicine Middle Aged musculoskeletal system medicine.disease Calcium ATPase Sarcoplasmic Reticulum Endocrinology cardiovascular system Cardiology Calmodulin-Binding Proteins Female Calcium Channels |
| Zdroj: | Molecular and cellular biochemistry. |
| ISSN: | 0300-8177 |
| Popis: | Previous studies on sarcoplasmic reticulum calcium release channel (ryanodine receptor) demonstrated that protein levels are unchanged in myocardium from hearts with end-stage failing dilated cardiomyopathy. In ischemic cardiomyopathy, ryanodine receptor mRNA levels were shown to be decreased but no data on protein levels are available. Accordingly, protein levels of ryanodine receptor, calsequestrin, and sarcoplasmic reticulum calcium-ATPase (SR-Ca(2+)-ATPase) were measured by Western blot analysis in nonfailing human myocardium (n = 7) and in end-stage failing myocardium due to ischemic cardiomyopathy (n = 14). Protein levels of calsequestrin which is the major sarcoplasmic reticulum calcium storage protein were similar in nonfailing myocardium and in myocardium from end-stage failing hearts with ischemic cardiomyopathy. Ryanodine receptor protein levels, normalized to total protein or calsequestrin were also unchanged in ischemic cardiomyopathy. In contrast, protein levels of SR-Ca(2+)-ATPase normalized to total protein or calsequestrin were decreased by 31 and 30%, respectively (p0.05). The data indicate that (1) sarcoplasmic reticulum calcium uptake sites are decreased relative to the release sites in ischemic cardiomyopathy, and (2) alterations of sarcoplasmic proteins are similar in ischemic and dilated cardiomyopathy. |
| Databáze: | OpenAIRE |
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