EH-myomesin splice isoform is a novel marker for dilated cardiomyopathy.

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Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_EF7FFFC60C7E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
EH-myomesin splice isoform is a novel marker for dilated cardiomyopathy.
Périodique
Basic Research in Cardiology
Auteur(s)
Schoenauer Roman, Emmert Maximilian Y., Felley Allison, Ehler Elisabeth, Brokopp Chad, Weber Benedikt, Nemir Mohamed, Faggian Giuseppe G., Pedrazzini Thierry, Falk Volkmar, Hoerstrup Simon P., Agarkova Irina
ISSN
1435-1803 (Electronic)
ISSN-L
0300-8428
Statut éditorial
Publié
Date de publication
2011
Volume
106
Numéro
2
Pages
233-247
Langue
anglais
Résumé
The M-band is the prominent cytoskeletal structure that cross-links the myosin and titin filaments in the middle of the sarcomere. To investigate M-band alterations in heart disease, we analyzed the expression of its main components, proteins of the myomesin family, in mouse and human cardiomyopathy. Cardiac function was assessed by echocardiography and compared to the expression pattern of myomesins evaluated with RT-PCR, Western blot, and immunofluorescent analysis. Disease progression in transgenic mouse models for dilated cardiomyopathy (DCM) was accompanied by specific M-band alterations. The dominant splice isoform in the embryonic heart, EH-myomesin, was strongly up-regulated in the failing heart and correlated with a decrease in cardiac function (R = -0.86). In addition, we have analyzed the expressions of myomesins in human myocardial biopsies (N = 40) obtained from DCM patients, DCM patients supported by a left ventricular assist device (LVAD), hypertrophic cardiomyopathy (HCM) patients and controls. Quantitative RT-PCR revealed that the EH-myomesin isoform was up-regulated 41-fold (P < 0.001) in the DCM patients compared to control patients. In DCM hearts supported by a LVAD and HCM hearts, the EH-myomesin expression was comparable to controls. Immunofluorescent analyses indicate that EH-myomesin was enhanced in a cell-specific manner, leading to a higher heterogeneity of the myocytes' cytoskeleton through the myocardial wall. We suggest that the up-regulation of EH-myomesin denotes an adaptive remodeling of the sarcomere cytoskeleton in the dilated heart and might serve as a marker for DCM in mouse and human myocardium.
Mots-clé
Dilated cardiomyopathy, Heart failure, Sarcomere cytoskeleton, M-band, Myomesin, sarcomeric m-band, heart-failure, muscle, protein, titin, identification, expression, gene, stiffness, catenin
Pubmed
Web of science
Open Access
Oui
Création de la notice
04/04/2011 15:47
Dernière modification de la notice
09/05/2019 3:12
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