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Published on: July 31, 2019
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression
Cíntia Júnia Monteiro1, Suianne Letícia Antunes Mota1, Lívia de Figueiredo Diniz1
1Departamento de Ciências Biológicas, Instituto de Ciências Exatas e Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
Insights
Chagas disease affects the heart. In Trypanosoma cruzi-infected cells, miRNA-190b reduces cell viability by decreasing PTEN protein expression, a key regulator.
Area of Science:
- Parasitology
- Molecular Biology
- Cardiovascular Research
Background:
- Chagas disease, caused by Trypanosoma cruzi, is a significant Latin American health issue impacting the heart.
- The molecular mechanisms of cardiomyocyte response to T. cruzi infection, especially post-entry, remain unclear.
- Phosphatidylinositol-3 kinase (PI3K) signaling is implicated in parasitic establishment, with PTEN acting as a negative regulator.
Purpose of the Study:
- To investigate the role of PTEN and microRNAs (miRNAs) in T. cruzi-infected cardiomyocytes.
- To elucidate the molecular mechanisms underlying PTEN modulation in Chagas disease pathogenesis.
Main Methods:
- Infection of H9c2 cardiomyoblast cells with the T. cruzi Berenice 62 strain.
- Investigation of specific microRNA (miRNA) expression profiles post-infection.
- Analysis of PTEN protein expression and its correlation with cellular viability.
Main Results:
- A specific miRNA, miRNA-190b, was identified in T. cruzi-infected cells.
- miRNA-190b expression was found to negatively correlate with PTEN protein levels.
- Reduced PTEN expression by miRNA-190b was associated with decreased cellular viability in infected cells.
Conclusions:
- miRNA-190b plays a role in modulating PTEN expression in T. cruzi-infected cardiomyocytes.
- This interaction contributes to reduced cellular viability, offering insights into Chagas disease pathogenesis.
- Targeting miRNA-190b or PTEN may represent potential therapeutic strategies for Chagas disease.
Abstract:
Chagas disease, which is caused by the intracellular protozoan Trypanosoma cruzi, is a serious health problem in Latin America. The heart is one of the major organs affected by this parasitic infection. The pathogenesis of tissue remodelling, particularly regarding cardiomyocyte behaviour after parasite infection, and the molecular mechanisms that occur immediately following parasite entry into host cells are not yet completely understood. Previous studies have reported that the establishment of parasitism is connected to the activation of the phosphatidylinositol-3 kinase (PI3K), which controls important steps in cellular metabolism by regulating the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate. Particularly, the tumour suppressor PTEN is a negative regulator of PI3K signalling. However, mechanistic details of the modulatory activity of PTEN on Chagas disease have not been elucidated. To address this question, H9c2 cells were infected with T. cruzi Berenice 62 strain and the expression of a specific set of microRNAs (miRNAs) were investigated. Our cellular model demonstrated that miRNA-190b is correlated to the decrease of cellular viability rates by negatively modulating PTEN protein expression in T. cruzi-infected cells.
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