Differential protein expression profiling of myocardial tissue in a mouse model of hypertrophic cardiomyopathy.

Abstract:

:Hypertrophic cardiomyopathy (HCM) is a genetic disorder caused by mutations in genes encoding sarcomere proteins. The mechanisms involved in the development of cardiac hypertrophy and heart failure remain poorly understood. Global proteomic profiling was used to study the cardiac proteome of mice predisposed to developing HCM. Hearts from three groups of mice (n=3 hearts per group) were studied: non-transgenic (NTG) and cardiac-specific transgenic models over-expressing either the normal (TnI(WT)) or a mutant cardiac troponin I gene (Gly203Ser; TnI(G203S)). Two-dimensional gel electrophoresis (2-DE) coupled with tandem mass spectrometry was used to identify proteins. Image analysis was performed using Progenesis SameSpots. A total of 34 proteins with at least a twofold change in the TnI(G203S) mouse model were identified. Alterations were detected in components involved in energy production, Ca(2+) handling, and cardiomyocyte structure. Expression level changes in cytoskeletal and contractile proteins were well represented in the study, including the intermediate filament protein desmin, which was further investigated in two additional physiological and pathological settings, i.e., exercise treatment, and severe heart failure in a novel double-mutant TnI-203/MHC-403 model of HCM. This study highlights the potential role of tissue proteomic profiling for mapping proteins, which may be critical in cardiac dysfunction and progression to heart failure in HCM.

journal_name

J Mol Cell Cardiol

authors

Lam L,Tsoutsman T,Arthur J,Semsarian C

doi

10.1016/j.yjmcc.2009.08.015

subject

Has Abstract

pub_date

2010-05-01 00:00:00

pages

1014-22

issue

5

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(09)00338-1

journal_volume

48

pub_type

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