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High-throughput phenotypic assessment of cardiac physiology in four commonly used inbred mouse strains
Authors:Kristin Moreth  Ralf Fischer  Helmut Fuchs  Valérie Gailus-Durner  Wolfgang Wurst  Hugo A. Katus  Raffi Bekeredjian  Martin Hrabě de Angelis
Affiliation:1. Institute of Experimental Genetics and the German Mouse Clinic, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
2. Institute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
3. Technische Universit?t München, Lehrstuhl für Entwicklungsgenetik, c/o Helmholtz Zentrum München, Neuherberg, Germany
4. MPI für Psychiatrie, Munich, Germany
5. DZNE, German Center for Neurodegenerative Diseases, Munich, Germany
6. Department of Medicine III, University of Heidelberg, Heidelberg, Germany
7. Lehrstuhl für Experimentelle Genetik, Technische Universit?t München, Freising-Weihenstephan, Germany
8. German Center for Diabetes Research, Neuherberg, Germany
9. Institute of Experimental Genetics and the German Mouse Clinic, Neuherberg, Germany
Abstract:Mice with genetic alterations are used in heart research as model systems of human diseases. In the last decade there was a marked increase in the recognition of genetic diversity within inbred mouse strains. Increasing numbers of inbred mouse strains and substrains and analytical variation of cardiac phenotyping methods require reproducible, high-throughput methods to standardize murine cardiovascular physiology. We describe methods for non-invasive, reliable, easy and fast to perform echocardiography and electrocardiography on awake mice. This method can be used for primary screening of the murine cardiovascular system in large-scale analysis. We provide insights into the physiological divergence of C57BL/6N, C57BL/6J, C3HeB/FeJ and 129P2/OlaHsd mouse hearts and define the expected normal values. Our report highlights that compared to the other three strains tested C57BL/6N hearts reveal features of heart failure such as hypertrophy and reduced contractile function. We found several features of the mouse ECG to be under genetic control and obtained several strain-specific differences in cardiac structure and function.
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