-Tropomyosin mutations AspAsn and GluGly affect cardiac function in transgenic rats in different ways
نویسندگان
چکیده
Dirk Wernicke,* Corinna Thiel,* Corina M. Duja-Isac, Kirill V. Essin, Matthias Spindler, Derek J. R. Nunez, Ralph Plehm, Niels Wessel, Annette Hammes, Robert-J. Edwards, Andrea Lippoldt, Ute Zacharias, Hinrik Strömer, Stefan Neubauer, Michael J. Davies, Ingo Morano, and Ludwig Thierfelder Max-Delbrück Center for Molecular Medicine, 13 092 Berlin; Clinic of Internal Medicine, Julius-Maximilians University, 97 080 Würzburg; and Franz Volhard Clinic, Charite of the Humboldt University, 13125 Berlin, Germany; Section on Clinical Pharmacology, Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN; and St. George’s Hospital Medical School, London SW17 ORE, United Kingdom
منابع مشابه
Autonomic cardiac control in animal models of cardiovascular diseases II. Variability analysis in transgenic rats with alpha-tropomyosin mutations Asp175Asn and Glu180Gly.
Animal models of cardiovascular diseases allow to investigate relevant pathogenetic mechanisms in detail. In the present study, the mutations Asp175Asn and Glu180Gly in alpha-tropomyosin (TPM1), known cause familiar hypertrophic cardiomyopathy (FHC) were studied for changes in hemodynamic parameters and spontaneous baroreflex regulation in transgenic rats in comparison to transgenic and non-tra...
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Myocardial interstitial fibrosis is an important contributor to the development of heart failure. Type 3 p90 ribosomal S6 kinase (RSK3) was recently shown to be required for concentric myocyte hypertrophy under in vivo pathological conditions. However, the role of RSK family members in myocardial fibrosis remains uninvestigated. Transgenic expression of α-tropomyosin containing a Glu180Gly muta...
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AIM Mutations in a sarcomeric protein can cause hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM), the opposite ends of a spectrum of phenotypic responses of the heart to mutations. We posit the contracting phenotypes could result from differential effects of the mutant proteins on interactions among the sarcomeric proteins. To test the hypothesis, we generated transgenic mice e...
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Familial hypertrophic cardiomyopathy (FHC) is a disease caused by mutations in contractile proteins of the sarcomere. Our laboratory developed a mouse model of FHC with a mutation in the thin filament protein alpha-tropomyosin (TM) at amino acid 180 (Glu180Gly). The hearts of these mice exhibit dramatic systolic and diastolic dysfunction, and their myofilaments demonstrate increased calcium sen...
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