Miosge, Nicolai

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Baranowsky, A."],["dc.contributor.author","Mokkapati, S."],["dc.contributor.author","Wickenhauser, C."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Krieg, Thomas"],["dc.contributor.author","Nischt, R."],["dc.date.accessioned","2018-11-07T10:56:16Z"],["dc.date.available","2018-11-07T10:56:16Z"],["dc.date.issued","2005"],["dc.format.extent","A17"],["dc.identifier.isi","000231862600097"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49975"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","35th Annual Meeting of the European-Society-for-Dermatological-Research"],["dc.relation.eventlocation","Tubingen, GERMANY"],["dc.relation.issn","0022-202X"],["dc.title","Role of the basement membrane proteins nidogen-1 and-2 for skin physiology and pathology"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","211"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Logo Cells Tissues Organs"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","192"],["dc.contributor.author","Zhu, Huiyong"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Schulz, Jutta"],["dc.contributor.author","Schliephake, Henning"],["dc.date.accessioned","2018-08-20T11:34:30Z"],["dc.date.available","2018-08-20T11:34:30Z"],["dc.date.issued","2010"],["dc.description.abstract","The aim of the present study was to analyze the effect of 3 different expansion media on the expression of marker genes of mesenchymal differentiation (bone, cartilage, fat) as well as apoptosis and senescence during repeated passaging in human bone marrow stromal cells (hBMSCs) in order to identify potential expansion strategies for the use of these cells into tissue-engineered growth of bone. Medium 1 (EGF, PDGF, low Glc, 2% FCS) was associated with the highest proliferation rate compared to medium 2 (β-mercaptoethanol, high Glc DMEM, 15% FCS) and medium 3 (low Glc DMEM, 10% FCS). Real time RT-PCR indicated the lowest levels of expression of osteonectin, core binding factor-α 1, lipoprotein lipase and cartilage oligo matrix protein in medium-1 cultures as compared to media 2 and 3. Early passages expressed higher levels of peroxisome proliferator-activator receptor-γ2 in medium 1 than in media 2 and 3, whereas no difference of Sox-9 expression was noticed among the 3 media. Expression of apoptosis- and senescence-related genes (Bax, BCL-2 and P16INK4a) exhibited the lowest level of Bax/BCL-2 ratio and P16INK4a gene expression of hBMSC in medium 1. In conclusion, the replacement of FCS by recombinant EGF and PDGF promoted rapid proliferation of hBMSCs without inducing differentiation of hBMSCs. It also inhibited expression of apoptosis-related genes and limited replicative senescence during repeated passaging. Media with the lowest possible FCS content and replacement by EGF and PDGF thus should be used for 2D culturing during expansion of hBMSCs, whereas β-mercaptoethanol and high concentrations of FCS can help to commence osteogenic differentiation."],["dc.identifier.doi","10.1159/000313417"],["dc.identifier.pmid","20407225"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15417"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1422-6421"],["dc.relation.eissn","1422-6405"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Regulation of multilineage gene expression and apoptosis during in vitro expansion of human bone marrow stromal cells with different cell culture media"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1375"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Clinical Oral Investigations"],["dc.bibliographiccitation.lastpage","1384"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Batschkus, Sarah"],["dc.contributor.author","Cingoez, Goekhan"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Kirschneck, Christian"],["dc.contributor.author","Meyer-Marcotty, Philipp"],["dc.contributor.author","Lenz, Christof"],["dc.date.accessioned","2020-12-10T14:11:03Z"],["dc.date.available","2020-12-10T14:11:03Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1007/s00784-017-2213-0"],["dc.identifier.eissn","1436-3771"],["dc.identifier.issn","1432-6981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70949"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","A new albumin-depletion strategy improves proteomic research of gingival crevicular fluid from periodontitis patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","482"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Ryu, M. I."],["dc.contributor.author","Migliorini, Adriana"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Shankland, Stuart"],["dc.contributor.author","Brinkkoetter, Paul T."],["dc.contributor.author","Hagmann, Henning"],["dc.contributor.author","Romagnani, Paola"],["dc.contributor.author","Liapis, Helen"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2018-11-07T09:02:32Z"],["dc.date.available","2018-11-07T09:02:32Z"],["dc.date.issued","2012"],["dc.description.abstract","Glomerular crescents are most common in rapidly progressive glomerulonephritis but also occur in noninflammatory chronic glomerulopathies; thus, factors other than inflammation should trigger crescent formation, eg vascular damage and plasma leakage. Here we report that Alport nephropathy in Col4A3-deficient Sv129 mice is complicated by diffuse and global crescent formation in which proliferating parietal epithelial cells are the predominant cell type. Laminin staining and transmission and acellular scanning electron microscopy of acellular glomeruli documented disruptions and progressive disintegration of the glomerular basement membrane in Col4A3-deficient mice. FITC-dextran perfusion further revealed vascular leakage from glomerular capillaries into Bowman's space, further documented by fibrin deposits in the segmental crescents. Its pathogenic role was validated by showing that the fibrinolytic activity of recombinant urokinase partially prevented crescent formation. In addition, in vitro studies confirmed an additional mitogenic potential of serum on murine and human parietal epithelial cells. Furthermore, loss of parietal cell polarity and unpolarized secretion of extracellular matrix components were evident within fibrocellular crescents. Among 665 human Alport nephropathy biopsies, crescent formation was noted in 0.4%. We conclude that glomerular vascular injury and GBM breaks cause plasma leakage which triggers a wound healing programme involving the proliferation of parietal cells and their loss of polarity. This process can trigger cellular and fibrocellular crescent formation even in the absence of cellular inflammation and rupture of the Bowman's capsule. Copyright (C) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.4046"],["dc.identifier.isi","000313949800007"],["dc.identifier.pmid","22553158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24705"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3417"],["dc.title","Plasma leakage through glomerular basement membrane ruptures triggers the proliferation of parietal epithelial cells and crescent formation in non-inflammatory glomerular injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1691"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular and Cellular Biology"],["dc.bibliographiccitation.lastpage","1699"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Ko, Y. P."],["dc.contributor.author","Kobbe, B."],["dc.contributor.author","Nicolae, C."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Paulsson, M."],["dc.contributor.author","Wagener, R."],["dc.contributor.author","Aszodi, A."],["dc.date.accessioned","2018-11-07T10:51:30Z"],["dc.date.available","2018-11-07T10:51:30Z"],["dc.date.issued","2004"],["dc.description.abstract","Matrilin-3 belongs to the matrilin family of extracellular matrix (ECM) proteins and is primarily expressed in cartilage. Mutations in the gene encoding human matrilin-3 (MATN-3) lead to autosomal dominant skeletal disorders, such as multiple epiphyseal dysplasia (MED), which is characterized by short stature and early-onset osteoarthritis, and bilateral hereditary microepiphyseal dysplasia, a variant form of MED characterized by pain in the hip and knee joints. To assess the function of matrilin-3 during skeletal development, we have generated Matn-3 null mice. Homozygous mutant mice appear normal, are fertile, and show no obvious skeletal malformations. Histological and ultrastructural analyses reveal endochondral bone formation indistinguishable from that of wild-type animals. Northern blot, immunohistochemical, and biochemical analyses indicated no compensatory upregulation of any other member of the matrilin family. Altogether, our findings suggest functional redundancy among matrilins and demonstrate that the phenotypes of MED disorders are not caused by the absence of matrilin-3 in cartilage ECM."],["dc.identifier.doi","10.1128/MCB.24.4.1691-1699.2004"],["dc.identifier.isi","000188744000023"],["dc.identifier.pmid","14749384"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48907"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0270-7306"],["dc.title","Matrilin-3 is dispensable for mouse skeletal growth and development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1399"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Expert Opinion on Biological Therapy"],["dc.bibliographiccitation.lastpage","1405"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Koelling, Sebastian"],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-11-07T11:22:40Z"],["dc.date.available","2018-11-07T11:22:40Z"],["dc.date.issued","2009"],["dc.description.abstract","Enhancing the regeneration potential of hyaline cartilage tissue remains a great challenge. During embryonic development, some of the cells of the inner cell mass will turn into the mesoderm. This will be the founder of the mesenchymal cells in connective tissues of adult life, such as bone, tendon, muscle, and cartilage. Some of these embryonic mesenchymal cells are believed not to differentiate, but reside in each of the tissues. These are now collectively described as adult mesenchymal stem cells, which are thought to be capable of repairing injured tissue. We will briefly summarize the current knowledge about stem cell-related cells in cartilage tissue and carefully discuss the potential of the cell population we described recently as a starting-point for a regenerative therapy for osteoarthritis. We found that repair tissue from human articular cartilage during the late stages of osteoarthritis harbors a unique progenitor cell population, termed chondrogenic progenitor cells (CPC). These exhibit stem cell characteristics combined with a high chondrogenic potential. They offer new insights into the biology of progenitor cells and may be relevant in the development of novel therapeutic approaches for a cell-based therapy for late stages of osteoarthritis."],["dc.identifier.doi","10.1517/14712590903246370"],["dc.identifier.isi","000271454300005"],["dc.identifier.pmid","19793003"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6059"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56025"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1471-2598"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Stem cell therapy for cartilage regeneration in osteoarthritis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","67"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Matrix Biology"],["dc.bibliographiccitation.lastpage","85"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Schmitz, Markus"],["dc.contributor.author","Niehoff, Anja"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Smyth, Neil"],["dc.contributor.author","Paulsson, Mats"],["dc.contributor.author","Zaucke, Frank"],["dc.date.accessioned","2018-11-07T11:17:51Z"],["dc.date.available","2018-11-07T11:17:51Z"],["dc.date.issued","2008"],["dc.description.abstract","In humans, mutations in cartilage oligomeric matrix protein (COMP) cause autosomal dominantly inherited skeletal dysplasias. We have generated transgenic mouse lines to study the role of mutant D469 Delta COMP in the pathogenesis of pseudoachondroplasia. Biochemical characterization of cartilage tissue demonstrated that transgenic and endogenous COMP subunits were able to form mixed, pentameric molecules in vivo. Mutant COMP was more difficult to extract than the wildtype protein, suggesting an altered anchorage within the matrix. Although both transgenic wildtype and mutant COMP were detected throughout the growth plate, mutant molecules were restricted to the pericellular matrix while wildtype COMP showed a uniform distribution throughout the extracellular matrix. Mice expressing the mutant transgene showed a slight gender specific growth retardation. In mutant animals, the columnar organization in the growth plate was disturbed, proteoglycans were lost and improperly formed collagen fibrils were observed. In some chondrocytes the endoplasmic reticulum was dilated, most probably due to an impaired secretion of mutant COMP similar to that observed in patients. Later in development, the growth plate was irregularly shaped and prematurely invaded by bony tissue. In addition, a fusion of the third and fourth sternebrae was frequently observed. (c) 2007 Elsevier B.V./International Society of Matrix Biology. All rights reserved."],["dc.identifier.doi","10.1016/j.matbio.2007.08.001"],["dc.identifier.isi","000253798800001"],["dc.identifier.pmid","17889519"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54911"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1569-1802"],["dc.relation.issn","0945-053X"],["dc.title","Transgenic mice expressing D469 Delta mutated cartilage oligomeric matrix protein (COMP) show growth plate abnormalities and sternal malformations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","177"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Journal of Molecular Histology"],["dc.bibliographiccitation.lastpage","184"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Roediger, Matthias"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gersdorff, Nikolaus"],["dc.date.accessioned","2018-08-20T11:49:34Z"],["dc.date.available","2018-08-20T11:49:34Z"],["dc.date.issued","2010"],["dc.description.abstract","Laminins are the major glycoproteins present in all basement membranes. Previously, we showed that perlecan is present during human development. Although an overview of mRNA-expression of the laminin beta1 and beta2 chains in various developing fetal organs is already available, a systematic localization of the laminin beta1 and beta2 chains on the protein level during embryonic and fetal human development is missing. Therefore, we studied the immunohistochemical expression and tissue distribution of the laminin beta1 and beta2 chains in various developing embryonic and fetal human organs between gestational weeks 8 and 12. The laminin beta1 chain was ubiquitously expressed in the basement membrane zones of the brain, ganglia, blood vessels, liver, kidney, skin, pancreas, intestine, heart and skeletal system. Furthermore, the laminin beta2 chain was present in the basement membrane zones of the brain, ganglia, skin, heart and skeletal system. The findings of this study support and expand upon the theory that these two laminin chains are important during human development."],["dc.identifier.doi","10.1007/s10735-010-9275-5"],["dc.identifier.pmid","20552257"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15420"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1567-2387"],["dc.relation.eissn","1567-2379"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Tissue distribution of the laminin β1 and β2 chain during embryonic and fetal human development"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII S0945-053X(02)00070-7"],["dc.bibliographiccitation.firstpage","611"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Matrix Biology"],["dc.bibliographiccitation.lastpage","621"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Sasaki, T."],["dc.contributor.author","Timpl, R."],["dc.date.accessioned","2018-11-07T09:53:49Z"],["dc.date.available","2018-11-07T09:53:49Z"],["dc.date.issued","2002"],["dc.description.abstract","Previous studies have shown that inhibition of nidogen-laminin binding interferes with basement membrane stabilization in various mouse organ cultures while no overt phenotype has been observed following inactivation of the nidogen-1 gene in mice. We have now used recombinant mouse nidogen-1 and nidogen-2 in order to evaluate a possible compensation between the two isoforms in the knock-out mice. Essentially, a comparable in vitro binding of nidogens-1 and -2 to the same laminin-1 chain structure and to several other basement membrane proteins has been revealed. Quantitative radioimmuno-assays have demonstrated high concentrations of nidogen-1 exceeding those of laminin gamma1 and nidogen-2 by factors of 5 and 20-50, respectively, in tissue extracts of wild-type mice. A three- to sevenfold increase in nidogen-2 was observed in heart and muscle of mice with nidogen-1 deficiency and confirmed by a similar increase in the intensity of immunogold staining of these tissues. However, a few of the tissues from mice with the gene knock-out still contained some nidogen-1-like immunoreactivity (1% of wild-type). Furthermore, both nidogen isoforms showed a similar distribution in various organs during embryonic development which, however, as shown previously, changed in some adult tissues. The data support the nidogen-2 compensation hypothesis to explain the limited phenotype observed following elimination of the nidogen-1 gene. (C) 2002 Elsevier Science B.V. and International Society of Matrix Biology. All rights reserved."],["dc.identifier.doi","10.1016/S0945-053X(02)00070-7"],["dc.identifier.isi","000179928600007"],["dc.identifier.pmid","12475645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36411"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0945-053X"],["dc.title","Evidence of nidogen-2 compensation for nidogen-1 deficiency in transgenic mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1342"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cellular Biochemistry"],["dc.bibliographiccitation.lastpage","1355"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Ponce, M. L."],["dc.contributor.author","Koelling, Sebastian"],["dc.contributor.author","Kluever, A."],["dc.contributor.author","Heinemann, D. E. H."],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Frosch, Karl-Heinz"],["dc.contributor.author","Schuetze, N."],["dc.contributor.author","Hufner, A."],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2018-11-07T11:13:34Z"],["dc.date.available","2018-11-07T11:13:34Z"],["dc.date.issued","2008"],["dc.description.abstract","Knowledge of the basic mechanisms controlling osteogenesis and adipogenesis might provide new insights into the prevention of osteoporosis and age-related osteopenia. With the help of magnetic cell sorting and fluorescence activated cell sorting (FACS), osteoblastic subpopulations of mesenchymal progenitor cells were characterized. Alkaline phosphatase (AP) negative cells expressed low levels of osteoblastic and adipocytic markers. AP positive cells expressed adipocytic markers more strongly than the AP negative cell populations, thus suggesting that committed osteoblasts exhibit a greater adipogenic potential. AP negative cells differentiated to the mature osteoblastic phenotype, as demonstrated by increased AP-activity and osteocalcin secretion under standard osteogenic culture conditions. Surprisingly, this was accompanied by increased expression of adipocytic gene markers such as peroxisome proliferator-activated receptor-gamma 2, lipoprotein lipase and fatty acid binding protein. The induction of adipogenic markers was suppressed by transforming growth factor-beta 1 (TGF-beta 1) and promoted by bone morphogenetic protein 2 (BMP-2). Osteogenic culture conditions including BMP-2 induced both the formation of mineralized nodules and cytoplasmic lipid vacuoles. Upon immunogold electron microscopic analysis, osteoblastic and adipogenic marker proteins were detectable in the same cell. Our results suggest that osteogenic and adipogenic differentiation in human mesenchymal progenitor cells might not be exclusively reciprocal, but rather, a parallel event until late during osteoblast development."],["dc.identifier.doi","10.1002/jcb.21711"],["dc.identifier.isi","000257567300018"],["dc.identifier.pmid","18286543"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6248"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53928"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0730-2312"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Coexpression of osteogenic and adipogenic differentiation markers in selected subpopulations of primary human mesenchymal progenitor cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]