RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23902766http://www.w3.org/2000/01/rdf-schema#comment"Idiopathic pulmonary fibrosis is a devastating lung disorder of unknown etiology. Although its pathogenesis is unclear, considerable evidence supports an important role of aberrantly activated alveolar epithelial cells (AECs), which produce a large variety of mediators, including several matrix metalloproteases (MMPs), which participate in fibroblast activation and lung remodeling. MMP-1 has been shown to be highly expressed in AECs from idiopathic pulmonary fibrosis lungs although its role is unknown. In this study, we explored the role of MMP-1 in several AECs functions. Mouse lung epithelial cells (MLE12) transfected with human Mmp-1 showed significantly increased cell growth and proliferation at 36 and 48 h of culture (p < 0.01). Also, MMP-1 promoted MLE12 cell migration through collagen I, accelerated wound closing, and protected cells from staurosporine- and bleomycin-induced apoptosis compared with mock cells (p < 0.01). MLE12 cells expressing human MMP-1 showed a significant repression of oxygen consumption ratio compared with the cells with the empty vector. As under hypoxic conditions hypoxia-inducible factor-1α (HIF-1α) mediates a transition from oxidative to glycolytic metabolism, we analyzed activation of HIF-1α. Ηigher activation of this factor was detected in MMP-1-transfected cells under normoxia and hypoxia. Likewise, a significant decrease of both total and mitochondrial reactive oxygen species was observed in MMP-1-transfected cells. Paralleling these findings, attenuation of MMP-1 expression by shRNA in A549 (human) AECs markedly reduced proliferation and migration (p < 0.01) and increased the oxygen consumption ratio. These findings indicate that epithelial expression of MMP-1 inhibits mitochondrial function, increases HIF-1α expression, decreases reactive oxygen species production, and contributes to a proliferative, migratory, and anti-apoptotic AEC phenotype."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m113.459784"xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Ortiz-Quintero B."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Ramirez R."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Selman M."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Chandel N.S."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Pardo A."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Maldonado M."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Cisneros J."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Anso E."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/author"Herrera I."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/pages"25964-25975"xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/title"Matrix metalloproteinase (MMP)-1 induces lung alveolar epithelial cell migration and proliferation, protects from apoptosis, and represses mitochondrial oxygen consumption."xsd:string
http://purl.uniprot.org/citations/23902766http://purl.uniprot.org/core/volume"288"xsd:string
http://purl.uniprot.org/citations/23902766http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23902766
http://purl.uniprot.org/citations/23902766http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23902766
http://purl.uniprot.org/uniprot/#_A5GZ69-mappedCitation-23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23902766
http://purl.uniprot.org/uniprot/#_B4DN15-mappedCitation-23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23902766
http://purl.uniprot.org/uniprot/#_B4DW26-mappedCitation-23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23902766
http://purl.uniprot.org/uniprot/#_L8EC95-mappedCitation-23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23902766
http://purl.uniprot.org/uniprot/#_Q53G95-mappedCitation-23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23902766
http://purl.uniprot.org/uniprot/#_Q53G96-mappedCitation-23902766http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23902766