Sadowski, Boguslawa

[["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","324"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cell Stem Cell"],["dc.bibliographiccitation.lastpage","335"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Koelling, Sebastian"],["dc.contributor.author","Kruegel, Jenny"],["dc.contributor.author","Irmer, Malte"],["dc.contributor.author","Path, Jan Ragnar"],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Miro, Xavier"],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-11-07T08:30:48Z"],["dc.date.available","2018-11-07T08:30:48Z"],["dc.date.issued","2009"],["dc.description.abstract","The regeneration of diseased hyaline cartilage continues to be a great challenge, mainly because degeneration-caused either by major injury or by age-related processes-can overextend the tissue's self-renewal capacity. We show that repair tissue from human articular cartilage during the late stages of osteoarthritis harbors a unique progenitor cell population, termed chondrogenic progenitor cells (CPCs). These exhibit stem cell characteristics such as clonogenicity, multipotency, and migratory activity. The isolated CPCs, which exhibit a high chondrogenic potential, were shown to populate diseased tissue ex vivo. Moreover, downregulation of the osteogenic transcription factor runx-2 enhanced the expression of the chondrogenic transcription factor sox-9. This, in turn, increased the matrix synthesis potential of the CPCs without altering their migratory capacity. Our results offer new insights into the biology of progenitor cells in the context of diseased cartilage tissue. Our work may be relevant in the development of novel therapeutics for the later stages of osteoarthritis."],["dc.description.sponsorship","Deutsche Arthrose Stiftung; Medical Faculty, Goettingen University"],["dc.identifier.doi","10.1016/j.stem.2009.01.015"],["dc.identifier.isi","000265162700009"],["dc.identifier.pmid","19341622"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6060"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16977"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1934-5909"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Migratory Chondrogenic Progenitor Cells from Repair Tissue during the Later Stages of Human Osteoarthritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1422"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Arthritis & Rheumatism"],["dc.bibliographiccitation.lastpage","1432"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Kruegel, Jenny"],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-11-07T11:15:18Z"],["dc.date.available","2018-11-07T11:15:18Z"],["dc.date.issued","2008"],["dc.description.abstract","Objective. To investigate the presence and function of nidogen-1 and nidogen-2 in healthy human cartilage and in late-stage osteoarthritis (OA) cartilage. Methods. The location and quantity of nidogen-1 and nidogen-2 protein and messenger RNA were determined in cartilage tissue obtained from healthy donors and from patients with late-stage knee OA. Samples were analyzed by immunohistochemistry, in situ hybridization, and real-time reverse transcription-polymerase chain reaction. Adhesion and inhibition assays, a preembedding method, fluorescence-activated cell sorting, and ultrastructural investigations with integrins were also carried out. Results. Developing tissue from human embryos showed strong staining for both nidogens in condensed mesenchyme and in rib anlagen. Homogeneous staining for nidogen-1 was observed in the extracellular matrix of healthy articular cartilage, whereas nidogen-2 was localized pericellularly. In late-stage OA cartilage, expression of nidogen-1 was decreased pericellularly around diseased chondrocytes, whereas nidogen-2 was increased. However, both nidogens had strongly increased levels around elongated chondrocytes, especially in areas of deep surface fissures. In vitro, both nidogens functioned as adhesion proteins for cells from the OA defect. In vivo, colocalizations with integrins alpha v and beta 1 as well as internalization of nidogens by chondrocytes in vitro were observed. Conclusion. Nidogens are involved in human limb development. They occur in healthy articular cartilage and show increased expression, primarily around elongated chondrocytes, in OA cartilage. Therefore, the activities of nidogens might be a sign of cartilage regeneration in late-stage OA. Furthermore, the adhesive character of nidogens, specifically as adhesion proteins for chondrocytes from late-stage OA, as well as the enhanced chondrocyte-nidogen interaction in OA indicate that both proteins play a key role in the pathogenesis of OA and either could be applied as a diagnostic marker."],["dc.identifier.doi","10.1002/art.23480"],["dc.identifier.isi","000255848400025"],["dc.identifier.pmid","18438862"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54339"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0004-3591"],["dc.title","Nidogen-1 and nidogen-2 in healthy human cartilage and in late-stage osteoarthritis cartilage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]