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Published on: September 15, 2018
Differential protein expression profiling of myocardial tissue in a mouse model of hypertrophic cardiomyopathy
Lien Lam1, Tatiana Tsoutsman, Jonathan Arthur
1Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Sydney, Australia.
Insights
Global proteomic profiling revealed significant protein alterations in mice with hypertrophic cardiomyopathy (HCM). These changes impact energy production, calcium handling, and cardiomyocyte structure, offering insights into HCM progression.
Area of Science:
- Cardiovascular Biology
- Proteomics
- Genetics
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart muscle disease.
- The underlying mechanisms of HCM-induced cardiac hypertrophy and heart failure are not fully understood.
Purpose of the Study:
- To investigate cardiac proteome alterations in a mouse model of HCM.
- To identify proteins critical for cardiac dysfunction in HCM.
Main Methods:
- Global proteomic profiling using 2D gel electrophoresis and mass spectrometry.
- Analysis of cardiac tissue from non-transgenic and transgenic mice expressing normal or mutant cardiac troponin I (TnI(G203S)).
Main Results:
- Identified 34 proteins with significant expression changes in the TnI(G203S) HCM mouse model.
- Detected alterations in proteins involved in energy production, Ca(2+) handling, and cardiomyocyte structure.
- Observed changes in cytoskeletal and contractile proteins, including desmin.
Conclusions:
- Proteomic profiling is a valuable tool for identifying proteins involved in cardiac dysfunction in HCM.
- Alterations in specific proteins may play a critical role in HCM progression and heart failure.
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.
