| http://purl.uniprot.org/citations/36672165 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/36672165 | http://www.w3.org/2000/01/rdf-schema#comment | "Melanoma inhibitory activity/cartilage-derived retinoicacid-sensitive protein (MIA/CD-RAP) is a protein expressed and secreted by chondrocytes and cartilaginous tissues. MIA/CD-RAP-deficient mice develop milder osteoarthritis than wildtype mice. In this study, we investigated MIA/CD-RAP downstream targets to explain this reduced disease development. As a possible mediator, we could detect matrix metalloproteinase 13 (MMP13), and the influence of MIA/CD-RAP on MMP13 regulation was analyzed in vitro using SW1353 chondrosarcoma cells and primary chondrocytes. The femoral head cartilage of WT and MIA/CD-RAP -/-mice were cultured ex vivo to further investigate MMP13 activity. Finally, osteoarthritis was surgically induced via DMM in C57BL/6 mice, and the animals were treated with an MIA/CD-RAP inhibitory peptide by subcutaneously implanted pellets. MMP13 was regulated by MIA/CD-RAP in SW1353 cells, and MIA/CD-RAP -/-murine chondrocytes showed less expression of MMP13. Further, IL-1β-treated MIA/CD-RAP -/-chondrocytes displayed less MMP13 expression and activity. Additionally, MIA/CD-RAP-deficient ex vivo cultured cartilage explants showed less MMP13 activity as well as reduced cartilage degradation. The mice treated with the MIA/CD-RAP inhibitory peptide showed less osteoarthritis development. Our findings revealed MIA/CD-RAP as a new regulator of MMP13 and highlighted its role as a potential new target for osteoarthritis therapy."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.org/dc/terms/identifier | "doi:10.3390/cells12020229"xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Bosserhoff A."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Schubert T."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Riechers A."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Gurbiel S."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Lichtblau A."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Rottensteiner-Brandl U."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/author | "Staebler S."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/name | "Cells"xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/pages | "229"xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/title | "MIA/CD-RAP Regulates MMP13 and Is a Potential New Disease-Modifying Target for Osteoarthritis Therapy."xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://purl.uniprot.org/core/volume | "12"xsd:string |
| http://purl.uniprot.org/citations/36672165 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/36672165 |
| http://purl.uniprot.org/citations/36672165 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/36672165 |
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| http://purl.uniprot.org/uniprot/#_Q3U2N6-mappedCitation-36672165 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/36672165 |
| http://purl.uniprot.org/uniprot/#_Q6GX98-mappedCitation-36672165 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/36672165 |
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| http://purl.uniprot.org/uniprot/#_Q61865-mappedCitation-36672165 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/36672165 |