The expression of SR calcium transport ATPase and the Na(+)/Ca(2+)Exchanger are antithetically regulated during mouse cardiac development and in Hypo/hyperthyroidism
Autor: | Thomas D. Reed, Mark Ver Heyen, Frank Wuytack, Muthu Periasamy, Alla Zilberman, Gopal J. Babu, Yong Ji |
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Rok vydání: | 2000 |
Předmět: |
Genetically modified mouse
medicine.medical_specialty Thyroid Hormones ATPase Calcium-Transporting ATPases Hyperthyroidism Sodium-Calcium Exchanger Mice Hypothyroidism Internal medicine Gene expression medicine Animals Molecular Biology Regulation of gene expression Sodium-calcium exchanger biology Endoplasmic reticulum Gene Expression Regulation Developmental Heart Phospholamban Transport protein Isoenzymes Sarcoplasmic Reticulum Endocrinology Muscle Fibers Fast-Twitch biology.protein Cardiology and Cardiovascular Medicine |
Zdroj: | Journal of molecular and cellular cardiology. 32(3) |
ISSN: | 0022-2828 |
Popis: | The mouse has been used extensively for generating transgenic animal models to study cardiovascular disease. Recently, a number of transgenic mouse models have been created to investigate the importance of sarcoplasmic reticulum (SR) Ca(2+)transport proteins in cardiac pathophysiology. However, the expression and regulation of cardiac SR Ca(2+)ATPase and other Ca(2+)transport proteins have not been studied in detail in the mouse. In this study, we used multiplex RNase mapping analysis to determine SERCA2, phospholamban (PLB), and Na(+)/Ca(2+)-exchanger (NCX-1) gene expression throughout mouse heart development and in hypo/hyperthyroid animals. Our results demonstrate that the expression of SERCA2 and PLB mRNA increase eight-fold from fetal to adult stages, indicating that SR function increases with heart development. In contrast, the expression of the Na(+)/Ca(2+)-exchanger gene is two-fold higher in fetal heart compared to adult. Our study also makes the important observation that in hypothyroidic hearts the NCX-1 mRNA and protein levels were upregulated, whereas the SERCA2 mRNA/protein levels were downregulated. In hyperthyroidic hearts, however, an opposite response was identified. These findings are important and point out that the expression of NCX-1 is regulated antithetically to that of SERCA2 during heart development and in response to alterations in thyroid hormone levels. |
Databáze: | OpenAIRE |
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