Open AccessDifferential interactions of thin filament proteins in two cardiac troponin T mouse models of hypertrophic and dilated cardiomyopathies
Author(s) -
Raffaella Lombardi,
Achim Bell,
Vinitha Senthil,
Jasvinder Sidhu,
Michela Noseda,
Robert Roberts,
Ali J. Marian
Publication year - 2008
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvn078
Subject(s) - troponin complex , myofibril , troponin t , troponin , actin , medicine , tropomyosin , hypertrophic cardiomyopathy , dilated cardiomyopathy , genetically modified mouse , cardiology , heart failure , biology , transgene , microbiology and biotechnology , gene , biochemistry , myocardial infarction
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 expressing either cardiac troponin T (cTnT)-Q92 or cTnT-W141, known to cause HCM and DCM, respectively, in the heart.
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