Miosge, Nicolai

[["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.lastpage","10"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Martin, Maria"],["dc.contributor.author","Kruegel, Jenny"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Temme, Johanna"],["dc.contributor.author","Eckes, Beate"],["dc.contributor.author","Müller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2019-07-09T11:52:48Z"],["dc.date.available","2019-07-09T11:52:48Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Integrins are important cellular receptors for collagens. Within the glomerulus, podocytes regulate the integrity of the glomerular basement membrane (GBM) by sensing the presence of collagen and regulating collagen IV synthesis. The present study evaluates the role of integrin a2 (ITGA2) in cell-matrix interaction. Methods and Results: ITGA2-deficient mice had normal renal function but moderate proteinuria and enhanced glomerular and tubulointerstitial matrix deposition. Electron microscopy demonstrated irregular podocyte-matrix interaction, causing pathological protrusions towards the urinary (podocyte) side of the GBM. These characteristic subepithelial bulges mimic the renal phenotype of mice, which are deficient in another collagen receptor, discoidin domain receptor (DDR)1. Using immunogold staining, ITGA2 expression was found to localize to the basolateral site of the podocyte foot processes. ITGA2-deficient mice overexpressed transforming growth factor (TGF)b and connective tissue growth factor (CTGF) compared with wild-type mice. Using in situ hybridization, tubular cells were found to be the primary site of TGFb synthesis and podocytes the source of CTGF in ITGA2- deficient mice. Conclusion: These findings support our hypothesis that both these collagen receptors (ITGA2 and DDR1) play a similar role within the kidney. Further, cell-matrix interaction via collagen receptors seems to be crucial for maintenance of normal GBM architecture and function. Targeting collagen receptors such as ITGA2 might be a new form of treatment for progressive fibrotic diseases."],["dc.identifier.doi","10.1186/1755-1536-3-19"],["dc.identifier.fs","575629"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60281"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/6905 but duplicate"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Integrin a2-deficient mice provide insights into specific functions of collagen receptors in the kidney"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","31"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Oral Biosciences"],["dc.bibliographiccitation.lastpage","45"],["dc.bibliographiccitation.volume","51"],["dc.contributor.author","Roediger, Matthias"],["dc.contributor.author","Miró, Xavier"],["dc.contributor.author","Geffers, Robert"],["dc.contributor.author","Irmer, Malte"],["dc.contributor.author","Huels, Alfons"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gersdorff, Nikolaus"],["dc.date.accessioned","2019-07-09T11:52:27Z"],["dc.date.available","2019-07-09T11:52:27Z"],["dc.date.issued","2009"],["dc.description.abstract","The purpose of this study was to compare gene expression profiles of peri-implantitis and periodontitis to elucidate potential differences at the molecular level. With the help of microarray analysis, genome-wide gene expression of inflamed peri-implant granulation tissue, inflamed and healthy periodontal tissues (n=48 patients) were compared and the data were validated by real-time reverse transcription polymerase chain reaction. After highlighting different gene classes, we focused on the extracellular matrix-receptor interaction pathway and gene expression of extracellular matrix molecules, their receptors and matrix degrading enzymes. Only genes of non-fibril-forming collagens (types IV, VI, VII, and Q) were increased in peri-implantitis compared to periodontitis, whereas the expressions of two fibril-forming collagens (types III and K) were decreased in peri-implantitis, which suggested that peri-implant tissue re-models faster than periodontal tissue in vivo. Furthermore, cathepsin D and cathepsin S seem to participate in the destruction of peri-implant connective tissue. Despite their clinical similarities, the present investigation demonstrated that peri-implantitis and periodontitis are two different disease entities at least at the messanger ribonucleic acid level. The data provide insight for future studies aimed at dissecting the pathogenesis of peri-implant inflammation."],["dc.identifier.doi","10.2330/joralbiosci.51.31"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4310"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60194"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Profiling of Differentially Expressed Genes in Peri-implantitis and Periodontitis in vivo by Microarray Analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","228"],["dc.bibliographiccitation.journal","European cells & materials"],["dc.bibliographiccitation.lastpage","241"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Docheva, D."],["dc.contributor.author","Padula, D."],["dc.contributor.author","Popov, C."],["dc.contributor.author","Weishaupt, P."],["dc.contributor.author","Prägert, M."],["dc.contributor.author","Miosge, N."],["dc.contributor.author","Hickel, R."],["dc.contributor.author","Böcker, W."],["dc.contributor.author","Clausen-Schaumann, H."],["dc.contributor.author","Schieker, M."],["dc.date.accessioned","2019-07-10T08:13:36Z"],["dc.date.available","2019-07-10T08:13:36Z"],["dc.date.issued","2010"],["dc.description.abstract","Periodontal ligament (PDL) can be obtained from patients undergoing orthodontic treatment. PDL contains progenitor cells that can be expanded and differentiated towards several mesenchymal lineages in vitro. Furthermore, PDL-derived cells have been shown to generate bone- and PDL-like structures in vivo. Thus, PDL cells, combined with suitable biomaterials, represent a promising tool for periodontitis-related research and PDL engineering. Here, a new PDL cell line using lentiviral gene transfer of human telomerase reverse transcriptase (hTERT) was created. HTERT-expressing PDL cells showed similar morphology and population doubling time but an extended lifespan compared to the primary cells. In addition, PDL-hTERT cells expressed several characteristic genes and upon osteogenic stimulation produced a calcified matrix in vitro. When cultivated on two topographically different titanium scaffolds (MA and SLA), PDL-hTERT cells exhibited augmented spreading, survival and differentiation on smooth (MA) compared to rough (SLA) surfaces. These findings differ from previously reported osteoblast behaviour, but they are in agreement with the behaviour of chondrocytes and gingival fibroblasts, suggesting a very cell type-specific response to different surface textures. In summary, we report the testing of titanium biomaterials using a new PDL-hTERT cell line and propose this cell line as a useful model system for periodontitis research and development of novel strategies for PDL engineering."],["dc.identifier.fs","575631"],["dc.identifier.pmid","20473831"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61288"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1473-2262"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Establishment of immortalized periodontal ligament progenitor cell line and its behavioural analysis on smooth and rough titanium surface."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Dental Research Journal"],["dc.bibliographiccitation.lastpage","11"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Gersdorff, Nikolaus"],["dc.contributor.author","Miró, Xavier"],["dc.contributor.author","Roediger, Matthias"],["dc.contributor.author","Geffers, Robert"],["dc.contributor.author","Huels, Alfons"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Toepfer, Tanja"],["dc.date.accessioned","2019-07-10T08:12:53Z"],["dc.date.available","2019-07-10T08:12:53Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: In the periodontium, the functions of the cell populations regarding the host-mediated tissue destruction in health and disease are not well understood. The purpose of this study was to measure the expression of genes differentially expressed in chronically inflamed periodontal ligament (PDL) cells compared to healthy PDL cells. Methods: We compared the genome-wide gene expressions of chronically inflamed and healthy PDL cells by microarray analysis, and validated the data by real-time RT-PCR to identify the genes that might play distinct roles in chronic periodontal disease in vivo. Results: The expression rates of 14,239 genes were investigated and 3,165 of them were found differentially expressed by at least two-fold; the expression rates of 1,515 genes were significantly upregulated and the expression rates of 1,650 genes were significantly downregulated in inflamed PDL cells. Conclusion: We focused on mainly structural components, for example, laminins and integrins, as well as degrading enzymes, for example, MMPs and cathepsins. The molecular composition of the laminin network varies in chronically inflamed compared to healthy PDL cells in vivo. Furthermore, integrin alpha6beta4, together with laminin-332, might be involved in chronic periodontal inflammation. Diverse keratins were upregulated, indicating that the epithelial cell rests of Malassez might also be involved in chronic periodontitis. The microarray analysis has identified a profile of genes potentially involved in chronic periodontal inflammation in vivo."],["dc.identifier.fs","432816"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4309"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61070"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Gene Expression Analysis of Chronically Inflamed and Healthy Human Periodontal Ligament Cells in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]