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Microarray analysis of changes in gene expression in a murine model of chronic chagasic cardiomyopathy
Shankar Mukherjee1, Thomas J Belbin, David C Spray
1Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Insights
Chagas disease causes heart damage by altering gene expression. This study reveals key genetic changes in mice infected with Trypanosoma cruzi, offering insights into chagasic cardiomyopathy.
Area of Science:
- Cardiology
- Infectious Diseases
- Molecular Biology
Background:
- Chagas disease, caused by Trypanosoma cruzi, is a significant cause of cardiomyopathy in endemic areas.
- Infection leads to cardiac remodeling, congestive heart failure, and dilated cardiomyopathy.
Purpose of the Study:
- To investigate the gene expression profile changes in the heart following Trypanosoma cruzi infection.
- To understand the molecular mechanisms underlying chagasic heart disease pathogenesis.
Main Methods:
- Male C57BL/6 x 129sv mice were infected with Trypanosoma cruzi (Brazil strain).
- Histopathological examination and cardiac magnetic resonance imaging were performed.
- High-density microarrays (27,400 mouse cDNAs) were used to analyze myocardial mRNA expression.
Main Results:
- Infected mice showed chronic inflammation, vasculitis, and fibrosis in the myocardium 100 days post-infection.
- Cardiac magnetic resonance imaging confirmed significant heart dilation compared to controls.
- Microarray analysis identified differentially expressed genes involved in various cellular functions, including transcription, metabolism, and host defense.
Conclusions:
- Trypanosoma cruzi infection induces significant alterations in myocardial gene expression.
- These gene expression changes contribute to the cardiac remodeling and pathogenesis of chagasic heart disease.
- The study provides a comprehensive gene expression profile relevant to understanding Chagas disease cardiomyopathy.
Abstract:
Chagas' disease, caused by infection with Trypanosoma cruzi, is a major cause of cardiomyopathy in endemic regions. Infection leads to cardiac remodeling associated with congestive heart failure and dilated cardiomyopathy. In order to study the changes in the gene expression profile due to infection, C57BL/6 x 129sv male mice were infected with 1 x 10(3) trypomastigotes of the Brazil strain of T. cruzi. Histopathological examination of the myocardium revealed chronic inflammation, vasculitis and fibrosis 100 days post-infection. Cardiac magnetic resonance imaging revealed a significantly dilated heart compared with uninfected mice. The relative abundance or depletion of myocardial mRNAs was evaluated using high-density microarrays consisting of 27,400 mouse cDNAs, which were hybridized with fluorescent probes generated from mRNAs of T. cruzi infected and uninfected hearts. Differentially expressed genes were sorted according to their normalized expression patterns and functional groups including those involved in transcription, intracellular transport, structure/junction/adhesion or extracellular matrix, signaling, host defense, energetics, metabolism, cell shape and death. The regulated genes are interpreted in the pathogenesis of chagasic heart disease.
