Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1590/0074-02760150184 http://hdl.handle.net/11449/161097 |
Resumo: | 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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Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expressioncardiac cellular modelmicroRNAPTENTrypanosoma cruziChagas 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.Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)UFOPUniv Fed Ouro Preto, Inst Ciencias Exatas & Biol, Nucleo Pesquisa Ciencias Biol, Dept Ciencias Biol,Lab Doenca Chagas, Ouro Preto, MG, BrazilUniv Estadual Paulista, Inst Biociencias, Dept Biol, Lab Biol Mol, Rio Claro, SP, BrazilUniv Estadual Paulista, Inst Biociencias, Dept Biol, Lab Biol Mol, Rio Claro, SP, BrazilFAPEMIG: CBB-APQ-02351-10FAPEMIG: CBB-APQ-01700-11CNPq: 475586/2009-3Fundaco Oswaldo CruzUniv Fed Ouro PretoUniversidade Estadual Paulista (Unesp)Monteiro, Cintia JuniaAntunes Mota, Suianne LeticiaDiniz, Livia de FigueiredoBahia, Maria TerezinhaMoraes, Karen C. M. [UNESP]2018-11-26T16:19:07Z2018-11-26T16:19:07Z2015-12-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article996-1002application/pdfhttp://dx.doi.org/10.1590/0074-02760150184Memorias Do Instituto Oswaldo Cruz. Rio De Janeiro, Rj: Fundaco Oswaldo Cruz, v. 110, n. 8, p. 996-1002, 2015.0074-0276http://hdl.handle.net/11449/16109710.1590/0074-02760150184S0074-02762015000800996WOS:000367480800007S0074-02762015000800996.pdfWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengMemorias Do Instituto Oswaldo Cruz1,172info:eu-repo/semantics/openAccess2023-10-15T06:06:08Zoai:repositorio.unesp.br:11449/161097Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462023-10-15T06:06:08Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
title |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
spellingShingle |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression Monteiro, Cintia Junia cardiac cellular model microRNA PTEN Trypanosoma cruzi |
title_short |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
title_full |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
title_fullStr |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
title_full_unstemmed |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
title_sort |
Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression |
author |
Monteiro, Cintia Junia |
author_facet |
Monteiro, Cintia Junia Antunes Mota, Suianne Leticia Diniz, Livia de Figueiredo Bahia, Maria Terezinha Moraes, Karen C. M. [UNESP] |
author_role |
author |
author2 |
Antunes Mota, Suianne Leticia Diniz, Livia de Figueiredo Bahia, Maria Terezinha Moraes, Karen C. M. [UNESP] |
author2_role |
author author author author |
dc.contributor.none.fl_str_mv |
Univ Fed Ouro Preto Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Monteiro, Cintia Junia Antunes Mota, Suianne Leticia Diniz, Livia de Figueiredo Bahia, Maria Terezinha Moraes, Karen C. M. [UNESP] |
dc.subject.por.fl_str_mv |
cardiac cellular model microRNA PTEN Trypanosoma cruzi |
topic |
cardiac cellular model microRNA PTEN Trypanosoma cruzi |
description |
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. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-12-01 2018-11-26T16:19:07Z 2018-11-26T16:19:07Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1590/0074-02760150184 Memorias Do Instituto Oswaldo Cruz. Rio De Janeiro, Rj: Fundaco Oswaldo Cruz, v. 110, n. 8, p. 996-1002, 2015. 0074-0276 http://hdl.handle.net/11449/161097 10.1590/0074-02760150184 S0074-02762015000800996 WOS:000367480800007 S0074-02762015000800996.pdf |
url |
http://dx.doi.org/10.1590/0074-02760150184 http://hdl.handle.net/11449/161097 |
identifier_str_mv |
Memorias Do Instituto Oswaldo Cruz. Rio De Janeiro, Rj: Fundaco Oswaldo Cruz, v. 110, n. 8, p. 996-1002, 2015. 0074-0276 10.1590/0074-02760150184 S0074-02762015000800996 WOS:000367480800007 S0074-02762015000800996.pdf |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Memorias Do Instituto Oswaldo Cruz 1,172 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
996-1002 application/pdf |
dc.publisher.none.fl_str_mv |
Fundaco Oswaldo Cruz |
publisher.none.fl_str_mv |
Fundaco Oswaldo Cruz |
dc.source.none.fl_str_mv |
Web of Science reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
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1799964571354529792 |