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Robust Mitochondrial Isolation from Rodent Cardiac Tissue
Published on: August 23, 2024
Mitochondrial involvement in chronic chagasic cardiomyopathy
Alejandra Báez1, María Silvina Lo Presti, Héctor Walter Rivarola
1Instituto de Investigación en Ciencias de Salud Humana, Departamento de Ciencias de Salud y Educación, Universidad Nacional de La Rioja, La Rioja, Argentina. alejandralidiab@hotmail.com
Insights
Chronic Chagasic cardiopathy involves cardiac mitochondrial dysfunction. Trypanosoma cruzi strains differentially impact mitochondrial structure and function, influenced by parasite persistence and inflammation.
Area of Science:
- Cardiovascular Biology
- Parasitology
- Mitochondrial Medicine
Background:
- The exact mechanisms driving chronic Chagasic cardiopathy remain unclear.
- Inflammation and its mediators are suspected to directly harm cardiac cells.
Purpose of the Study:
- To investigate cardiac mitochondrial structure and function in chronic Chagasic myocardiopathy.
- To compare the effects of different Trypanosoma cruzi strains on cardiac mitochondria.
Main Methods:
- Studied mitochondrial structure and enzyme activity (citrate synthase, respiratory chain complexes I-IV) in mice infected with T. cruzi (Tulahuen or SGO Z12 strains) 365 days post-infection.
- Assessed parasite presence in cardiac and skeletal muscle.
Main Results:
- Complexes I-IV activity was altered differently by each T. cruzi strain (P<0.0001).
- Mitochondrial cristae disorganization and parasite persistence were noted in the Tulahuen group.
- Citrate synthase activity increased in both infected groups; mitochondrial structural changes occurred in 89% (Tulahuen) and 58% (SGO Z12) of mice.
Conclusions:
- Parasite persistence and inflammation contribute to cardiac mitochondrial structural and functional alterations in chronic Chagas disease.
- The specific T. cruzi strain dictates the nature of mitochondrial changes observed in chagasic cardiopathy.
Abstract:
The pathogenesis of chronic chagasic cardiopathy is still under discussion; there is considerable evidence that inflammatory infiltrates and their mediators have a direct effect on cardiac cells. Here we studied the structure and function of cardiac mitochondria in chronic chagasic myocardiopathy. Cardiac mitochondrial structure and enzyme activity of citrate synthase and complexes I to IV of the respiratory chain were studied in albino Swiss mice infected with Trypanosoma cruzi (Tulahuen strain or SGO Z12 isolate) on 365 days post-infection (dpi). The presence of parasites in cardiac and skeletal muscle was also investigated. The activity of complexes I to IV was altered in different ways, according to the strain employed (P<0.0001), in relation to the cristae disorganisation and the parasite persistence found in the Tulahuen group, and the chronic inflammatory process described in both groups; citrate synthase activity also increased in both infected groups. Changes in mitochondrial structure were detected in 89% of Tulahuen- and 58% of SGO Z12-infected mice. In this paper we demonstrate that parasite persistence and inflammation are likely to be involved in the structural and functional alterations in cardiac mitochondria from chronically T. cruzi-infected mice, demonstrating that the parasite strain determines different mitochondrial changes in chagasic cardiopathy.
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