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dc.contributor.authorGkretsi, Vasiliki
dc.contributor.authorPapanikolaou, Vassilis K.
dc.contributor.authorDubos, Stephanie
dc.contributor.authorPapathanasiou, Ioanna
dc.contributor.authorGiotopoulou, Nikolina
dc.contributor.authorValiakou, Vaia
dc.contributor.authorWu, Chuanyue
dc.contributor.authorMalizos, Konstantinos N.
dc.contributor.authorTsezou, Aspasia N.
dc.creatorGkretsi, Vasiliki
dc.date.accessioned2018-11-27T07:57:20Z
dc.date.available2018-11-27T07:57:20Z
dc.date.issued2013-01-11
dc.identifierSCOPUS_ID:84872296228
dc.identifier.issn0006291X
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84872296228&origin=inward
dc.identifier.urihttps://repo.euc.ac.cy/handle/123456789/1031
dc.description.abstractOsteoarthritis (OA) is a debilitating disease of the joints characterized by cartilage degradation but to date there is no available pharmacological treatment to inhibit disease progression neither is there any available biomarker to predict its development. In the present study, we examined the expression level and possible involvement of novel cell-ECM adhesion-related molecules such as Iintegrin Linked Kinase (ILK), PINCH, parvin, Mig-2 and Migfilin in OA pathogenesis using primary human articular chondrocytes from healthy individuals and OA patients. Our findings show that only ILK and Migfilin were upregulated in OA compared to the normal chondrocytes. Interestingly, Migfilin silencing in OA chondrocytes rather exacerbated than ameliorated the osteoarthritic phenotype, as it resulted in even higher levels of catabolic and hypertrophic markers while at the same time induced reduction in ECM molecules such as aggrecan. Furthermore, we also provide a link between Migfilin and β-catenin activation in OA chondrocytes, showing Migfilin to be inversely correlated with β-catenin. Thus, the present study emphasizes for the first time to our knowledge the role of Migfilin in OA and highlights the importance of cell-ECM adhesion proteins in OA pathogenesis.
dc.relation.ispartofBiochemical and Biophysical Research Communications
dc.titleMigfilin's elimination from osteoarthritic chondrocytes further promotes the osteoarthritic phenotype via β-catenin upregulation
elsevier.identifier.doi10.1016/j.bbrc.2012.12.008
elsevier.identifier.eid2-s2.0-84872296228
elsevier.identifier.piiS0006291X12023364
elsevier.identifier.scopusidSCOPUS_ID:84872296228
elsevier.volume430
elsevier.issue.identifier2
elsevier.coverdate2013-01-11
elsevier.coverdisplaydate11 January 2013
elsevier.openaccess0
elsevier.openaccessflagfalse
elsevier.aggregationtypeJournal


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