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http://purl.uniprot.org/citations/16825657http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16825657http://www.w3.org/2000/01/rdf-schema#comment"Matrix metalloproteinases (MMPs) are a family of extracellular proteases that are responsible for the degradation of the extracellular matrix during tissue remodeling. We have used a mouse model of allergen-induced airway remodeling to determine whether MMP-9 plays a role in airway remodeling. MMP-9-deficient and wild-type (WT) mice were repetitively challenged intranasally with ovalbumin (OVA) antigen to develop features of airway remodeling including peribronchial fibrosis and increased thickness of the peribronchial smooth muscle layer. OVA-challenged MMP-9-deficient mice had less peribronchial fibrosis and total lung collagen compared with OVA-challenged WT mice. There was no reduction in mucus expression, smooth muscle thickness, or airway responsiveness in OVA-challenged MMP-9-deficient compared with OVA-challenged WT mice. OVA-challenged MMP-9-deficient mice had reduced levels of bronchoalveolar lavage (BAL) regulated on activation, normal T cell expressed, and secreted (RANTES), as well as reduced numbers of BAL and peribronchial eosinophils compared with OVA-challenged WT mice. There were no significant difference in levels of BAL eotaxin, thymus- and activation-regulated chemokine (TARC), or macrophage-derived chemokine (MDC) in OVA-challenged WT compared with MMP-9-deficient mice. Overall, this study demonstrates that MMP-9 may play a role in mediating selected aspects of allergen-induced airway remodeling (i.e., modest reduction in levels of peribronchial fibrosis) but does not play a significant role in mucus expression, smooth muscle thickness, or airway responsiveness."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.org/dc/terms/identifier"doi:10.1152/ajplung.00305.2005"xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/author"Miller M."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/author"Cho J.Y."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/author"Lim D.H."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/author"Broide D.H."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/author"McElwain K."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/author"McElwain S."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/name"Am J Physiol Lung Cell Mol Physiol"xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/pages"L265-71"xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/title"Reduced peribronchial fibrosis in allergen-challenged MMP-9-deficient mice."xsd:string
http://purl.uniprot.org/citations/16825657http://purl.uniprot.org/core/volume"291"xsd:string
http://purl.uniprot.org/citations/16825657http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16825657
http://purl.uniprot.org/citations/16825657http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16825657
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http://purl.uniprot.org/uniprot/#_Q3UQ52-mappedCitation-16825657http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16825657
http://purl.uniprot.org/uniprot/#_Q6GXA2-mappedCitation-16825657http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16825657
http://purl.uniprot.org/uniprot/#_Q91ZS5-mappedCitation-16825657http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16825657
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http://purl.uniprot.org/uniprot/Q3UQ52http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/16825657