Schminke, Boris

[["dc.bibliographiccitation.firstpage","1081"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Cellular and Molecular Life Sciences"],["dc.bibliographiccitation.lastpage","1096"],["dc.bibliographiccitation.volume","71"],["dc.contributor.author","Schminke, Boris"],["dc.contributor.author","Muhammad, Hayat"],["dc.contributor.author","Bode, Christa"],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Gerter, Regina"],["dc.contributor.author","Gersdorff, Nikolaus"],["dc.contributor.author","Buergers, Ralf"],["dc.contributor.author","Monsonego-Ornan, Efrat"],["dc.contributor.author","Rosen, Vicki"],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-11-07T09:43:22Z"],["dc.date.available","2018-11-07T09:43:22Z"],["dc.date.issued","2014"],["dc.description.abstract","Discoidin domain receptor 1 (DDR-1)-deficient mice exhibited a high incidence of osteoarthritis (OA) in the temporomandibular joint (TMJ) as early as 9 weeks of age. They showed typical histological signs of OA, including surface fissures, loss of proteoglycans, chondrocyte cluster formation, collagen type I upregulation, and atypical collagen fibril arrangements. Chondrocytes isolated from the TMJs of DDR-1-deficient mice maintained their osteoarthritic characteristics when placed in culture. They expressed high levels of runx-2 and collagen type I, as well as low levels of sox-9 and aggrecan. The expression of DDR-2, a key factor in OA, was increased. DDR-1-deficient chondrocytes from the TMJ were positively influenced towards chondrogenesis by a three-dimensional matrix combined with a runx-2 knockdown or stimulation with extracellular matrix components, such as nidogen-2. Therefore, the DDR-1 knock-out mouse can serve as a novel model for temporomandibular disorders, such as OA of the TMJ, and will help to develop new treatment options, particularly those involving tissue regeneration."],["dc.identifier.doi","10.1007/s00018-013-1436-8"],["dc.identifier.isi","000331653900010"],["dc.identifier.pmid","23912900"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34171"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Basel"],["dc.relation.issn","1420-9071"],["dc.relation.issn","1420-682X"],["dc.title","A discoidin domain receptor 1 knock-out mouse as a novel model for osteoarthritis of the temporomandibular joint"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","410"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","186"],["dc.contributor.author","Schminke, Boris"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Bode, Christa"],["dc.contributor.author","Goldring, Mary B."],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-08-20T09:58:00Z"],["dc.date.available","2018-08-20T09:58:00Z"],["dc.date.issued","2016"],["dc.description.abstract","The aim of this study was to investigate the role of laminins and nidogen-2 in osteoarthritis (OA) and their potential to support chondrogenic differentiation. We applied immunohistochemistry, electron microscopy, siRNA, quantitative RT-PCR, Western blot, and proteome analysis for the investigation of cartilage tissue and isolated chondrocytes in three-dimensional culture obtained from patients with late-stage knee OA and nidogen-2 knockout mice. We demonstrate that subunits of laminins appear in OA cartilage and that nidogen-2-null mice exhibit typical osteoarthritic features. Chondrogenic progenitor cells (CPCs) produced high levels of laminin-α1, laminin-α5, and nidogen-2 in their pericellular matrix, and laminin-α1 enhanced collagen type II and reduced collagen type I expression by cultured CPCs. Nidogen-2 increased SOX9 gene expression. Knockdown of nidogen-2 reduced SOX9 expression, whereas it up-regulated RUNX2 expression. This study reveals that the influence of the pericellular matrix on CPCs is important for the expression of the major regulator transcription factors, SOX9 and RUNX2. Our novel findings that laminins and nidogen-2 drive CPCs toward chondrogenesis may help in the elucidation of new treatment strategies for cartilage tissue regeneration."],["dc.identifier.doi","10.1016/j.ajpath.2015.10.014"],["dc.identifier.pmid","26683663"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15413"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1525-2191"],["dc.title","Laminins and Nidogens in the Pericellular Matrix of Chondrocytes: Their Role in Osteoarthritis and Chondrogenic Differentiation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","789"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stem Cell Reports"],["dc.bibliographiccitation.lastpage","803"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Muhammad, Hayat"],["dc.contributor.author","Schminke, Boris"],["dc.contributor.author","Bode, Christa"],["dc.contributor.author","Roth, Moritz"],["dc.contributor.author","Albert, Julius"],["dc.contributor.author","von der Heyde, Silvia"],["dc.contributor.author","Rosen, Vicki"],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-08-20T12:45:38Z"],["dc.date.available","2018-08-20T12:45:38Z"],["dc.date.issued","2014"],["dc.description.abstract","Degeneration of the knee joint during osteoarthritis often begins with meniscal lesions. Meniscectomy, previously performed extensively after meniscal injury, is now obsolete because of the inevitable osteoarthritis that occurs following this procedure. Clinically, meniscus self-renewal is well documented as long as the outer, vascularized meniscal ring remains intact. In contrast, regeneration of the inner, avascular meniscus does not occur. Here, we show that cartilage tissue harvested from the avascular inner human meniscus during the late stages of osteoarthritis harbors a unique progenitor cell population. These meniscus progenitor cells (MPCs) are clonogenic and multipotent and exhibit migratory activity. We also determined that MPCs are likely to be controlled by canonical transforming growth factor β (TGF-β) signaling that leads to an increase in SOX9 and a decrease in RUNX2, thereby enhancing the chondrogenic potential of MPC. Therefore, our work is relevant for the development of novel cell biological, regenerative therapies for meniscus repair."],["dc.identifier.doi","10.1016/j.stemcr.2014.08.010"],["dc.identifier.pmid","25418724"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15440"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2213-6711"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Human Migratory Meniscus Progenitor Cells Are Controlled via the TGF-β Pathway"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]