Sadowski, Boguslawa

[["dc.bibliographiccitation.artnumber","1163"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Meschkat, Martin"],["dc.contributor.author","Steyer, Anna M."],["dc.contributor.author","Weil, Marie-Theres"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Piepkorn, Lars"],["dc.contributor.author","Agüi-Gonzalez, Paola"],["dc.contributor.author","Phan, Nhu Thi Ngoc"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Möbius, Wiebke"],["dc.date.accessioned","2022-04-01T10:00:48Z"],["dc.date.available","2022-04-01T10:00:48Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Myelin, the electrically insulating sheath on axons, undergoes dynamic changes over time. However, it is composed of proteins with long lifetimes. This raises the question how such a stable structure is renewed. Here, we study the integrity of myelinated tracts after experimentally preventing the formation of new myelin in the CNS of adult mice, using an inducible Mbp null allele. Oligodendrocytes survive recombination, continue to express myelin genes, but they fail to maintain compacted myelin sheaths. Using 3D electron microscopy and mass spectrometry imaging we visualize myelin-like membranes failing to incorporate adaxonally, most prominently at juxta-paranodes. Myelinoid body formation indicates degradation of existing myelin at the abaxonal side and the inner tongue of the sheath. Thinning of compact myelin and shortening of internodes result in the loss of about 50% of myelin and axonal pathology within 20 weeks post recombination. In summary, our data suggest that functional axon-myelin units require the continuous incorporation of new myelin membranes."],["dc.identifier.doi","10.1038/s41467-022-28720-y"],["dc.identifier.pii","28720"],["dc.identifier.pmid","35246535"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105516"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/458"],["dc.identifier.url","https://for2848.gwdguser.de/literature/publications/27"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","FOR 2848: Architektur und Heterogenität der inneren mitochondrialen Membran auf der Nanoskala"],["dc.relation","FOR 2848 | P08: Strukturelle und funktionale Veränderungen der inneren mitochondrialen Membran axonaler Mitochondrien in vivo in einem dymyelinisierenden Mausmodell"],["dc.relation.eissn","2041-1723"],["dc.relation.workinggroup","RG Möbius"],["dc.relation.workinggroup","RG Rizzoli (Quantitative Synaptology in Space and Time)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","White matter integrity in mice requires continuous myelin synthesis at the inner tongue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Zhao, Chao"],["dc.contributor.author","Cruz-Herranz, Andrés"],["dc.contributor.author","Ben Haim, Lucile"],["dc.contributor.author","Cordano, Christian"],["dc.contributor.author","Shiow, Lawrence R."],["dc.contributor.author","Kelley, Kevin W."],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Timmons, Garrett"],["dc.contributor.author","Pröbstel, Anne-Katrin"],["dc.contributor.author","Wright, Jackie N."],["dc.contributor.author","Sin, Jung Hyung"],["dc.contributor.author","Devereux, Michael"],["dc.contributor.author","Morrison, Daniel E."],["dc.contributor.author","Chang, Sandra M."],["dc.contributor.author","Sabeur, Khalida"],["dc.contributor.author","Green, Ari J."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Franklin, Robin JM."],["dc.contributor.author","Rowitch, David H."],["dc.date.accessioned","2018-11-15T12:52:25Z"],["dc.date.accessioned","2021-10-27T13:21:09Z"],["dc.date.available","2018-11-15T12:52:25Z"],["dc.date.available","2021-10-27T13:21:09Z"],["dc.date.issued","2018"],["dc.description.abstract","Glial support is critical for normal axon function and can become dysregulated in white matter (WM) disease. In humans, loss-of-function mutations of KCNJ10, which encodes the inward-rectifying potassium channel KIR4.1, causes seizures and progressive neurological decline. We investigated Kir4.1 functions in oligodendrocytes (OLs) during development, adulthood and after WM injury. We observed that Kir4.1 channels localized to perinodal areas and the inner myelin tongue, suggesting roles in juxta-axonal K+ removal. Conditional knockout (cKO) of OL-Kcnj10 resulted in late onset mitochondrial damage and axonal degeneration. This was accompanied by neuronal loss and neuro-axonal dysfunction in adult OL-Kcnj10 cKO mice as shown by delayed visual evoked potentials, inner retinal thinning and progressive motor deficits. Axon pathologies in OL-Kcnj10 cKO were exacerbated after WM injury in the spinal cord. Our findings point towards a critical role of OL-Kir4.1 for long-term maintenance of axonal function and integrity during adulthood and after WM injury."],["dc.identifier.doi","10.7554/eLife.36428"],["dc.identifier.pmid","30204081"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91997"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2050-084X"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Oligodendrocyte-encoded Kir4.1 function is required for axonal integrity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","889"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","899"],["dc.bibliographiccitation.volume","216"],["dc.contributor.author","Tarasenko, Daryna"],["dc.contributor.author","Barbot, Mariam"],["dc.contributor.author","Jans, Daniel C."],["dc.contributor.author","Kroppen, Benjamin"],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Heim, Gudrun"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Jakobs, Stefan"],["dc.contributor.author","Meinecke, Michael"],["dc.date.accessioned","2018-01-17T13:22:56Z"],["dc.date.available","2018-01-17T13:22:56Z"],["dc.date.issued","2017"],["dc.description.abstract","The inner membrane (IM) of mitochondria displays an intricate, highly folded architecture and can be divided into two domains: the inner boundary membrane adjacent to the outer membrane and invaginations toward the matrix, called cristae. Both domains are connected by narrow, tubular membrane segments called cristae junctions (CJs). The formation and maintenance of CJs is of vital importance for the organization of the mitochondrial IM and for mitochondrial and cellular physiology. The multisubunit mitochondrial contact site and cristae organizing system (MICOS) was found to be a major factor in CJ formation. In this study, we show that the MICOS core component Mic60 actively bends membranes and, when inserted into prokaryotic membranes, induces the formation of cristae-like plasma membrane invaginations. The intermembrane space domain of Mic60 has a lipid-binding capacity and induces membrane curvature even in the absence of the transmembrane helix. Mic60 homologues from α-proteobacteria display the same membrane deforming activity and are able to partially overcome the deletion of Mic60 in eukaryotic cells. Our results show that membrane bending by Mic60 is an ancient mechanism, important for cristae formation, and had already evolved before α-proteobacteria developed into mitochondria."],["dc.identifier.doi","10.1083/jcb.201609046"],["dc.identifier.pmid","28254827"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11711"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/9"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P01: Untersuchung der Unterschiede in der Zusammensetzung, Funktion und Position von individuellen MICOS Komplexen in einzelnen Säugerzellen"],["dc.relation","SFB 1190 | P12: Funktionelle Regulation der mitochondrialen Präsequenz-Translokase"],["dc.relation.eissn","1540-8140"],["dc.relation.orgunit","Institut für Zellbiochemie"],["dc.relation.workinggroup","RG Jakobs (Structure and Dynamics of Mitochondria)"],["dc.relation.workinggroup","RG Meinecke (Molecular Membrane Biology)"],["dc.rights","CC BY-NC-SA 4.0"],["dc.title","The MICOS component Mic60 displays a conserved membrane-bending activity that is necessary for normal cristae morphology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["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.journal","Movement Disorders"],["dc.contributor.author","Stuendl, Anne"],["dc.contributor.author","Kraus, Tanja"],["dc.contributor.author","Chatterjee, Madhurima"],["dc.contributor.author","Zapke, Björn"],["dc.contributor.author","Sadowski, Boguslawa"],["dc.contributor.author","Moebius, Wiebke"],["dc.contributor.author","Hobert, Markus A."],["dc.contributor.author","Deuschle, Christian"],["dc.contributor.author","Brockmann, Kathrin"],["dc.contributor.author","Schneider, Anja"],["dc.date.accessioned","2021-06-01T09:42:18Z"],["dc.date.available","2021-06-01T09:42:18Z"],["dc.date.issued","2021"],["dc.description.abstract","Background\r\n\r\nExtracellular vesicles are small vesicles that are released from many cells, including neurons. α-Synuclein has recently been described in extracellular vesicles derived from the central nervous system and may contribute to the spreading of disease pathology in α-synuclein-related neurodegeneration.\r\nObjectives\r\n\r\nWe aimed to examine the potential diagnostic value of α-synuclein in plasma extracellular vesicles from patients with Parkinson's disease (PD).\r\nMethods\r\n\r\nPreanalytical variables were studied to establish an optimized assay for preparation of plasma extracellular vesicles and detection of extracellular vesicle–derived α-synuclein. Plasma samples were obtained from 2 independent cohorts. The Tübingen cohort contained 96 patients with PD, 50 patients with dementia with Lewy bodies, 50 patients with progressive supranuclear palsy (PSP), and 42 healthy controls; the Kassel cohort included 47 patients with PD, 43 patients with dementia with Lewy bodies, and 36 controls with secondary parkinsonian syndromes. Extracellular vesicles were prepared from total plasma by size exclusion chromatography and quantified by nanoparticle tracking analysis, α-synuclein content was measured by an electrochemiluminescence assay.\r\nResults\r\n\r\nα-Synuclein concentration in plasma extracellular vesicles provided the best discrimination between PD, dementia with Lewy bodies, PSP, and healthy controls, with an area under the curve of 0.804 (PD vs dementia with Lewy bodies), 0.815 (PD vs. PSP), and 0.769 (PD vs healthy controls) in the Tübingen cohort. Results were validated in the Kassel cohort."],["dc.identifier.doi","10.1002/mds.28639"],["dc.identifier.pmid","34002893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85208"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/261"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1531-8257"],["dc.relation.issn","0885-3185"],["dc.relation.workinggroup","RG Möbius"],["dc.rights","CC BY 4.0"],["dc.title","α‐Synuclein in Plasma‐Derived Extracellular Vesicles Is a Potential Biomarker of Parkinson's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]