Improvement of defective sarcoplasmic reticulum Ca2+ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene
| Autor: | Frank Spillmann, Uwe Rehfeld, Martin Paul, Dirk Westermann, Michael Bader, Matthias Koch, Andreas Dendorfer, Christine Altmann, Heinz-Peter Schultheiss, Roland Vetter, Thomas Walther, Carsten Tschöpe |
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| Rok vydání: | 2004 |
| Předmět: |
medicine.medical_specialty
Calmodulin Bradykinin Gene Expression Calcium-Transporting ATPases Biology Biochemistry Ventricular Function Left Diabetes Mellitus Experimental Sarcoplasmic Reticulum Calcium-Transporting ATPases Animals Genetically Modified chemistry.chemical_compound Internal medicine Genetics medicine Animals Humans Phosphorylation Molecular Biology Calcium metabolism Ion Transport Endoplasmic reticulum Myocardium Calcium-Binding Proteins Streptozotocin Phospholamban Rats Sarcoplasmic Reticulum Endocrinology chemistry Reticular connective tissue cardiovascular system biology.protein Calcium Tissue Kallikreins circulatory and respiratory physiology Biotechnology medicine.drug |
| Zdroj: | FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 18(15) |
| ISSN: | 1530-6860 |
| Popis: | The bradykinin-forming enzyme kallikrein-1 is expressed in the heart. To examine whether contractile performance and sarcoplasmic reticulum Ca2+ transport of the diabetic heart can be rescued by targeting the kallikrein-kinin system, we studied left ventricular function and sarcoplasmic reticular Ca2+ uptake after induction of streptozotocin-induced diabetes mellitus in transgenic rats expressing the human tissue kallikrein-1 gene. Six weeks after a single injection of either streptozotocin (70 mg/kg ip) or vehicle, left ventricular performance was determined using a Millar-Tip catheter system. The Ca2+-transporting activity of reticulum-derived membrane vesicles was determined in left ventricular homogenates as oxalate-supported 45Ca2+ uptake. Western blot analysis was used to quantify the reticular Ca2+-ATPase SERCA2a, phospholamban, and the phosphorylation status of the latter. Contractile performance and Ca2+ uptake activity were similar in nondiabetic wild-type and transgenic rats. Severely diabetic wild-type animals exhibited impaired left ventricular performance and decreased reticular Ca2+ uptake (-39% vs. wild-type rats, P |
| Databáze: | OpenAIRE |
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