RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/26511729http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26511729http://www.w3.org/2000/01/rdf-schema#comment"Cardiac fibrosis is a complex pathological process that includes the abnormal proliferation of cardiac fibroblasts and deposition of the extracellular matrix (ECM) proteins and collagens. Methyl-CpG-binding protein 2 (MeCP2) is a multifunctional nuclear protein, and plays a key role in the fibrotic diseases. However, the potential role of MeCP2 in cardiac fibrosis remains unclear. We report that MeCP2 modulates cardiac fibrosis via down-regulation of dual-specificity phosphatase 5 (DUSP5), a nuclear phosphatase that negatively regulates prohypertrophic signaling by ERK1/2. MeCP2 is a critical participant in the epigenetic silencing of regulatory genes. Here, we found that down-regulation of DUSP5 in cardiac fibrosis is associated with MeCP2 over-expression. Treatment of cardiac fibroblasts with MeCP2-siRNA blocked proliferation. Knockdown of MeCP2 elevated DUSP5 expression in activated cardiac fibroblasts. Moreover, we investigated the effect of DUSP5 on the ERK1/2 activation. Our results demonstrated that MeCP2 modulates DUSP5 mediated activation of ERK1/2 in cardiac fibrosis. Taken together, these results indicated that MeCP2 acts as a key regulator of pathological cardiac fibrosis, promotes cardiac fibroblasts proliferation and fibrosis by down-regulation of DUSP5."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.org/dc/terms/identifier"doi:10.1016/j.ijbiomac.2015.10.076"xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/author"Hu W."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/author"Yang J.J."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/author"Tao H."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/author"Deng Z.Y."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/author"Shi K.H."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/name"Int J Biol Macromol"xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/pages"68-75"xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/title"MeCP2 regulation of cardiac fibroblast proliferation and fibrosis by down-regulation of DUSP5."xsd:string
http://purl.uniprot.org/citations/26511729http://purl.uniprot.org/core/volume"82"xsd:string
http://purl.uniprot.org/citations/26511729http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26511729
http://purl.uniprot.org/citations/26511729http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26511729
http://purl.uniprot.org/uniprot/#_A6JHW0-mappedCitation-26511729http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26511729
http://purl.uniprot.org/uniprot/#_A6JHW1-mappedCitation-26511729http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26511729
http://purl.uniprot.org/uniprot/#_O54838-mappedCitation-26511729http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26511729
http://purl.uniprot.org/uniprot/O54838http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26511729
http://purl.uniprot.org/uniprot/A6JHW0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26511729
http://purl.uniprot.org/uniprot/A6JHW1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26511729