Miró, Xavier

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The American Journal of Human Genetics"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Cichon, Sven"],["dc.contributor.author","Muehleisen, Thomas W."],["dc.contributor.author","Degenhardt, Franziska A."],["dc.contributor.author","Mattheisen, Manuel"],["dc.contributor.author","Miro, Xavier"],["dc.contributor.author","Strohmaier, Jana"],["dc.contributor.author","Steffens, Michael"],["dc.contributor.author","Meesters, Christian"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Weingarten, Moritz"],["dc.contributor.author","Priebe, Lutz"],["dc.contributor.author","Haenisch, Britta"],["dc.contributor.author","Alexander, Michael J."],["dc.contributor.author","Vollmer, Jennifer"],["dc.contributor.author","Breuer, Rene"],["dc.contributor.author","Schmael, Christine"],["dc.contributor.author","Tessmann, Peter"],["dc.contributor.author","Moebus, Susanne"],["dc.contributor.author","Wichmann, Heinz-Erich"],["dc.contributor.author","Schreiber, Stefan"],["dc.contributor.author","Mueller-Myhsok, Bertram"],["dc.contributor.author","Lucae, Susanne"],["dc.contributor.author","Jamain, Stephane"],["dc.contributor.author","Leboyer, Marion"],["dc.contributor.author","Bellivier, Frank"],["dc.contributor.author","Etain, Bruno"],["dc.contributor.author","Henry, Chantal"],["dc.contributor.author","Kahn, Jean-Pierre"],["dc.contributor.author","Heath, Simon"],["dc.contributor.author","Hamshere, Marian L."],["dc.contributor.author","O'Donovan, Michael C."],["dc.contributor.author","Owen, Michael J."],["dc.contributor.author","Craddock, Nick"],["dc.contributor.author","Schwarz, Markus"],["dc.contributor.author","Vedder, Helmut"],["dc.contributor.author","Kammerer-Ciernioch, Jutta"],["dc.contributor.author","Reif, Andreas"],["dc.contributor.author","Sasse, Johanna"],["dc.contributor.author","Bauer, Michael"],["dc.contributor.author","Hautzinger, Martin"],["dc.contributor.author","Wright, Adam"],["dc.contributor.author","Mitchell, Philip B."],["dc.contributor.author","Schofield, Peter R."],["dc.contributor.author","Montgomery, Grant W."],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Gordon, Scott D."],["dc.contributor.author","Martin, Nicholas G."],["dc.contributor.author","Gustafsson, Omar"],["dc.contributor.author","Andreassen, Ole A."],["dc.contributor.author","Djurovic, Srdjan"],["dc.contributor.author","Sigurdsson, Engilbert"],["dc.contributor.author","Steinberg, Stacy"],["dc.contributor.author","Stefansson, Hreinn"],["dc.contributor.author","Stefansson, Kari"],["dc.contributor.author","Kapur-Pojskic, Lejla"],["dc.contributor.author","Oruc, Liliana"],["dc.contributor.author","Rivas, Fabio"],["dc.contributor.author","Mayoral, Fermin"],["dc.contributor.author","Chuchalin, Alexander"],["dc.contributor.author","Babadjanova, Gulja"],["dc.contributor.author","Tiganov, Alexander S."],["dc.contributor.author","Pantelejeva, Galina"],["dc.contributor.author","Abramova, Lilia I."],["dc.contributor.author","Grigoroiu-Serbanescu, Maria"],["dc.contributor.author","Diaconu, Carmen C."],["dc.contributor.author","Czerski, Piotr M."],["dc.contributor.author","Hauser, Joanna"],["dc.contributor.author","Zimmer, Andreas"],["dc.contributor.author","Lathrop, Mark"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Wienker, Thomas F."],["dc.contributor.author","Schumacher, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Propping, Peter"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Noethen, Markus M."],["dc.date.accessioned","2018-11-07T08:58:10Z"],["dc.date.available","2018-11-07T08:58:10Z"],["dc.date.issued","2011"],["dc.format.extent","396"],["dc.identifier.doi","10.1016/j.ajhg.2011.03.001"],["dc.identifier.isi","000288589000019"],["dc.identifier.pmid","21353194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23581"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0002-9297"],["dc.title","Genome-wide Association Study Identifies Genetic Variation in Neurocan as a Susceptibility Factor for Bipolar Disorder (vol 88, pg 372, 2011)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","412"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Disease Models & Mechanisms"],["dc.bibliographiccitation.lastpage","418"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Miró, Xavier"],["dc.contributor.author","Zhou, Xunlei"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Kubisch, Christian"],["dc.contributor.author","Alvarez-Bolado, Gonzalo"],["dc.contributor.author","Gruss, Peter"],["dc.date.accessioned","2017-09-07T11:45:25Z"],["dc.date.available","2017-09-07T11:45:25Z"],["dc.date.issued","2009"],["dc.description.abstract","Polycomb proteins are epigenetic regulators of gene expression. Human central nervous system (CNS) malformations are congenital defects of the brain and spinal cord. One example of a human CNS malformation is Chiari malformation (CM), which presents as abnormal brainstem growth and cerebellar herniation, sometimes accompanied by spina bifida and cortical defects; it can occur in families. Clinically, CM ranges from an asymptomatic condition to one with incapacitating or lethal symptoms, including neural tube defects and hydrocephalus. However, no genes that are causally involved in any manifestation of CM or similar malformations have been identified. Here, we show that a pathway that involves Zac1 (also known as Plagl1 or Lot1) and controls neuronal proliferation is altered in mice that are heterozygous for the polycomb gene Suz12, resulting in a phenotype that overlaps with some clinical manifestations of the CM spectrum. Suz12 heterozygotes show cerebellar herniation and an enlarged brainstem, accompanied by occipital cortical alterations and spina bifida. Downward displacement of the cerebellum causes hydrocephalus in the most severely impaired cases. Although the involvement of polycomb genes in human disease is starting to be recognized, this is the first demonstration of their role in nervous system malformations. Our work strongly suggests that brain malformations such as CM can result from altered epigenetic regulation of genes involved in cell proliferation in the brain."],["dc.identifier.doi","10.1242/dmm.001602"],["dc.identifier.gro","3150365"],["dc.identifier.pmid","19535498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7122"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1754-8403"],["dc.title","Haploinsufficiency of the murine polycomb gene Suz12 results in diverse malformations of the brain and neural tube"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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.issue","11"],["dc.bibliographiccitation.journal","Human Gene Therapy"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Koelling, Sebastian"],["dc.contributor.author","Miro, Xavier"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Miosge, Nicolai"],["dc.date.accessioned","2018-11-07T11:22:42Z"],["dc.date.available","2018-11-07T11:22:42Z"],["dc.date.issued","2009"],["dc.format.extent","1403"],["dc.identifier.isi","000271441000164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56034"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mary Ann Liebert Inc"],["dc.publisher.place","New rochelle"],["dc.relation.conference","Combined Meeting of the 17th European-Society-of-Gene-and-Cell-Therapy/16th German-Society-for-Gene-Therapy/4th German-Society-for-Stem-Cell-Research"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1043-0342"],["dc.title","Migratory chondrogenic progenitor cells from late stages of osteoarthritis exhibit gender differences"],["dc.type","conference_abstract"],["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","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"]]