title: Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression.
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.
authors.affiliation: Departamento de Ciências Biológicas, Instituto de Ciências Exatas e Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
authors.forename: Cíntia Júnia
authors.initials: CJ
authors.lastname: Monteiro
authors.affiliation: Departamento de Ciências Biológicas, Instituto de Ciências Exatas e Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
authors.forename: Suianne Letícia Antunes
authors.initials: SL
authors.lastname: Mota
authors.affiliation: Departamento de Ciências Biológicas, Instituto de Ciências Exatas e Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
authors.forename: Lívia de Figueiredo
authors.initials: Lde F
authors.lastname: Diniz
authors.affiliation: Departamento de Ciências Biológicas, Instituto de Ciências Exatas e Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, MG, Brasil.
authors.forename: Maria Terezinha
authors.initials: MT
authors.lastname: Bahia
authors.affiliation: Departamento de Biologia, Instituto de Biociências, Universidade Estadual Paulista Júlio de Mesquita Filho, Rio Claro, SP, Brasil.
authors.forename: Karen C M
authors.initials: KC
authors.lastname: Moraes
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D002470:Cell Survival; D015536:Down-Regulation; D005562:Formazans; D017930:Genes, Reporter; D035683:MicroRNAs / Q000502:physiology*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000469:parasitology*; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism*; D010766:Phosphorylation; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013778:Tetrazolium Salts; D014349:Trypanosoma cruzi / Q000145:classification / Q000378:metabolism*
chemical_list: D005562:Formazans; C551254:MIRN190 microRNA, rat; D035683:MicroRNAs; D012333:RNA, Messenger; D013778:Tetrazolium Salts; C079782:MTT formazan; D051059:PTEN Phosphohydrolase