TY - JOUR
T1 - Microarray analysis of changes in gene expression in a murine model of chronic chagasic cardiomyopathy
AU - Mukherjee, Shankar
AU - Belbin, Thomas J.
AU - Spray, David C.
AU - Iacobas, Dumitru A.
AU - Weiss, Louis M.
AU - Kitsis, Richard N.
AU - Wittner, Murray
AU - Jelicks, Linda A.
AU - Scherer, Philip E.
AU - Ding, Aihao
AU - Tanowitz, Herbert B.
N1 - Funding Information:
Acknowledgements Supported by grant number AI-12770 (HBT), GM-61710 (AD), DK 55758 (PES), NS 42807 (DCS) and HL 07372 (HBT and DCS) from the US National Institutes of Health. The authors wish to thank Dr. Carl Nathan, Department of Microbiology and Immunology, Weill Medical College of Cornell University for his support. In addition we wish to thank Dr. Nicholas Socci, Department of Pathology and the staff of the Albert Einstein College of Medicine Microarray Facility for assistance with the microarrays and with data collection. The experiments comply with the current laws of the country in which the experiments were performed.
PY - 2003/10/1
Y1 - 2003/10/1
N2 - 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/6x129sv male mice were infected with 1×103 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.
AB - 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/6x129sv male mice were infected with 1×103 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.
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U2 - 10.1007/s00436-003-0937-z
DO - 10.1007/s00436-003-0937-z
M3 - Article
C2 - 12910413
AN - SCOPUS:10744221918
SN - 0932-0113
VL - 91
SP - 187
EP - 196
JO - Parasitology Research
JF - Parasitology Research
IS - 3
ER -