Related Experiment Video
Updated: Apr 9, 2026
Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs
Published on: June 23, 2022
MicroRNA Transcriptome Profiling in Heart of Trypanosoma cruzi-Infected Mice: Parasitological and Cardiological
Isabela Cunha Navarro1, Frederico Moraes Ferreira1, Helder I Nakaya2
1Laboratory of Immunology, Heart Institute (InCor), University of São Paulo School of Medicine, São Paulo, Brazil; Division of Clinical Immunology and Allergy, University of São Paulo School of Medicine, São Paulo, Brazil; Institute for Investigation in Immunology, iii-INCT, São Paulo, Brazil.
Insights
MicroRNAs (miRNAs) play a role in Chagas heart disease progression. Altered miRNA expression in mice correlates with parasite levels and cardiac dysfunction, suggesting their involvement in disease pathogenesis.
Area of Science:
- Cardiovascular Research
- Parasitology
- Molecular Biology
Background:
- Chagas disease, caused by Trypanosoma cruzi, leads to chronic cardiac complications in 30% of infected individuals.
- The mechanisms underlying Chagas heart disease, including myocarditis and fibrosis, remain largely undefined.
- Acute phase parasitemia and symptoms are linked to chronic cardiac disease severity.
Purpose of the Study:
- To investigate the role of microRNAs (miRNAs) in the progression of Chagas disease.
- To identify specific miRNAs deregulated during T. cruzi infection and their correlation with clinical parameters.
- To explore the potential contribution of miRNAs to Chagas heart disease pathogenesis.
Main Methods:
- Screening of 641 rodent miRNAs in mouse heart samples during acute T. cruzi infection.
- Analysis of miRNA expression at three time points post-infection.
- Computational analysis of miRNA gene targets and associated signaling pathways.
Main Results:
- Multiple miRNAs were significantly altered upon T. cruzi infection.
- Seventeen miRNAs were deregulated across all analyzed time points.
- Six miRNAs showed correlation with parasitemia and QT interval prolongation.
Conclusions:
- Specific miRNAs are significantly altered during T. cruzi infection in mice.
- These deregulated miRNAs are linked to key clinical parameters of Chagas disease.
- The findings provide a basis for understanding miRNA involvement in Chagas heart disease pathogenesis.
Abstract:
Chagas disease is caused by the parasite Trypanosoma cruzi, and it begins with a short acute phase characterized by high parasitemia followed by a life-long chronic phase with scarce parasitism. Cardiac involvement is the most prominent manifestation, as 30% of infected subjects will develop abnormal ventricular repolarization with myocarditis, fibrosis and cardiomyocyte hypertrophy by undefined mechanisms. Nevertheless, follow-up studies in chagasic patients, as well as studies with murine models, suggest that the intensity of clinical symptoms and pathophysiological events that occur during the acute phase of disease are associated with the severity of cardiac disease observed during the chronic phase. In the present study we investigated the role of microRNAs (miRNAs) in the disease progression in response to T. cruzi infection, as alterations in miRNA levels are known to be associated with many cardiovascular disorders. We screened 641 rodent miRNAs in heart samples of mice during an acute infection with the Colombiana T.cruzi strain and identified multiple miRNAs significantly altered upon infection. Seventeen miRNAs were found significantly deregulated in all three analyzed time points post infection. Among these, six miRNAs had their expression correlated with clinical parameters relevant to the disease, such as parasitemia and maximal heart rate-corrected QT (QTc) interval. Computational analyses identified that the gene targets for these six miRNAs were involved in networks and signaling pathways related to increased ventricular depolarization and repolarization times, important factors for QTc interval prolongation. The data presented here will guide further studies about the contribution of microRNAs to Chagas heart disease pathogenesis.
