ArticleMemorias do Instituto Oswaldo Cruz2015
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression.
Article in Memorias do Instituto Oswaldo Cruz, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Unraveling the role of miRNAs as biomarkers in Chagas cardiomyopathy: Insights into molecular pathophysiology.PLoS neglected tropical diseases · 2024Review
- Comparative microRNA profiling ofFrontiers in cellular and infection microbiology · 2023Article
- Immune and Genomic Analysis of Boxer Dog Breed and Its Relationship withVeterinary sciences · 2022Article
- Modulation of miR-145-5p and miR-146b-5p levels is linked to reduced parasite load in H9C2 Trypanosoma cruzi infected cardiomyoblasts.Scientific reports · 2022Article
- Circulating miR-146a as a possible candidate biomarker in the indeterminate phase of Chagas disease.Biological research · 2021Article
- Physical Exercise Training and Chagas Disease: Potential Role of MicroRNAs.Arquivos brasileiros de cardiologia · 2021Review
- Predicting host dependency factors of pathogens inComputational and structural biotechnology journal · 2021Article
- Integrated Analysis Reveals That miR-193b, miR-671, and TREM-1 Correlate With a Good Response to Treatment of Human Localized Cutaneous Leishmaniasis Caused byFrontiers in immunology · 2018Article
- TGF-β Targeted by miR-27a Modulates Anti-Parasite Responses of Immune System.Iranian journal of parasitologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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