A novel function for CUGBP2 in controlling the pro-inflammatory stimulus in H9c2 cells: Subcellular trafficking of messenger molecules

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dc.contributor.authorMoraes, Karen C. M. [UNESP]
dc.contributor.authorMonteiro, Cíntia Júnia
dc.contributor.authorPacheco-Soares, Cristina
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de Ouro Preto (UFOP)
dc.contributor.institutionUniversidade do Vale do Paraíba (UNIVAP)
dc.date.accessioned2014-05-27T11:29:40Z
dc.date.available2014-05-27T11:29:40Z
dc.date.issued2013-06-07
dc.description.abstractAccumulating evidence demonstrates that chronic inflammation plays an important role in heart hypertrophy and cardiac diseases. However, the fine-tuning of cellular and molecular mechanisms that connect inflammatory process and cardiac diseases is still under investigation. Many reports have demonstrated that the overexpression of the cyclooxygenase-2 (COX-2), a key enzyme in the conversion of arachidonic acid to prostaglandins and other prostanoids, is correlated with inflammatory processes. Increased level of prostaglandin E2 was also found in animal model of left ventricle of hypertrophy. Based on previous observations that demonstrated a regulatory loop between COX-2 and the RNA-binding protein CUGBP2, we studied cellular and molecular mechanisms of a pro-inflammatory stimulus in a cardiac cell to verify if the above two molecules could be correlated with the inflammatory process in the heart. A cellular model of investigation was established and H9c2 was used.We also demonstrated a regulatory connection between COX-2 and CUGBP2 in the cardiac cells. Based on a set of different assays including gene silencing and fluorescence microscopy, we describe a novel function for the RNA-binding protein CUGBP2 in controlling the pro-inflammatory stimulus: subcellular trafficking of messenger molecules to specific cytoplasmic stress granules to maintain homeostasis. © 2013 International Federation for Cell Biology.en
dc.description.affiliationDepartamento de Biologia Instituto de Biociências Universidade Estadual Paulista, Rio Claro, SP
dc.description.affiliationNúcleo de Pesquisa em Ciências Biológicas Biochemistry and Molecular Biology Laboratory Universidade Federal de Ouro Preto, Ouro Preto, MG
dc.description.affiliationCell Biology Laboratory Universidade do Vale do Paraíba Instituto de Pesquisa e Desenvolvimento, São Jose dos Campos, SP
dc.description.affiliationUnespDepartamento de Biologia Instituto de Biociências Universidade Estadual Paulista, Rio Claro, SP
dc.format.extent1129-1138
dc.identifierhttp://dx.doi.org/10.1002/cbin.10127
dc.identifier.citationCell Biology International, v. 37, n. 10, p. 1129-1138, 2013.
dc.identifier.doi10.1002/cbin.10127
dc.identifier.issn1065-6995
dc.identifier.issn1095-8355
dc.identifier.scopus2-s2.0-84884975690
dc.identifier.urihttp://hdl.handle.net/11449/75619
dc.identifier.wosWOS:000323932000011
dc.language.isoeng
dc.relation.ispartofCell Biology International
dc.relation.ispartofjcr1.936
dc.relation.ispartofsjr0,712
dc.relation.ispartofsjr0,712
dc.rights.accessRightsAcesso restrito
dc.sourceScopus
dc.subjectCellular homeostasis
dc.subjectCUGBP2
dc.subjectH9c2 cells
dc.subjectPro-inflammatory stimulus
dc.subjectStress granules
dc.subjectSubcellular translocation
dc.titleA novel function for CUGBP2 in controlling the pro-inflammatory stimulus in H9c2 cells: Subcellular trafficking of messenger moleculesen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
unesp.author.orcid0000-0002-0572-074X[3]
unesp.author.orcid0000-0002-3789-6432[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt

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