Siebert, Heike

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:35:31Z"],["dc.date.available","2018-11-07T10:35:31Z"],["dc.date.issued","2003"],["dc.format.extent","389"],["dc.identifier.isi","000185600700017"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45118"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","48th Annual Meeting of the German-Society-for-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","BERLIN, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Permanent axonal loss in EAE in WLDs mice occurs independently of Wallerian degeneration"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3401"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","3408"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Bitsch, Andreas"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2022-03-01T11:44:15Z"],["dc.date.available","2022-03-01T11:44:15Z"],["dc.date.issued","2001"],["dc.description.abstract","The present study investigated the fate of macrophages in peripheral nerves undergoing Wallerian degeneration, especially their disappearance from the injured nerves after phagocytosis of axonal and myelin debris. Wallerian degeneration was induced in adult male C57Bl/6 mice by transecting the right sciatic nerve. Five days after transection, the male sciatic nerves were transplanted into female recipient mice by placing them exactly parallel to the host sciatic nerves. Nerves of the female recipient mice were also transected to induce breakdown of the blood-nerve barrier in the host animal. Apoptosis was assessed by morphological, immunohistochemical (activated caspase-3), and molecular (DNA fragmentation) methods in transplanted, recipient, and in control nerves. A subpopulation of macrophages within the degenerating nerves died locally by apoptosis in each experiment. The fate of the male macrophages within the transplanted nerves and the host organism was investigated by in situ hybridization with a Y-chromosome-specific DNA probe (145SC5). In situ hybridization specifically stained cells within the transplanted male nerve. Y-chromosome-positive cells were detected not only inside the transplanted nerve, but also inside the female host nerve, the perineurial tissue, the local perineurial blood vessels, draining lymph nodes and the spleen of the female host, suggesting hematogenous as well as lymphatic elimination of macrophages from the injured nerve. These data indicate that local apoptosis and systemic elimination via circulation to the local lymph nodes and the spleen are involved in the disappearance of macrophages from the injured peripheral nervous system."],["dc.identifier.doi","10.1523/JNEUROSCI.21-10-03401.2001"],["dc.identifier.isi","000168409400016"],["dc.identifier.pmid","11331370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102973"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Macrophages Are Eliminated from the Injured Peripheral Nerve via Local Apoptosis and Circulation to Regional Lymph Nodes and the Spleen"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T11:24:45Z"],["dc.date.available","2018-11-07T11:24:45Z"],["dc.date.issued","2001"],["dc.format.extent","532"],["dc.identifier.isi","000171662200082"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56477"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","0001-6322"],["dc.title","Evidence for local and systemic elimination of macrophages from the injured peripheral nervous system"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","57"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Singh, Shailender"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Roemer, Shanu"],["dc.contributor.author","Maruschak, Brigitte"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T10:26:08Z"],["dc.date.available","2018-11-07T10:26:08Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. Methods: Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions. Furthermore, we studied the effects of Wallerian degeneration blockage on clinical severity, inflammatory pathology, acute axonal damage, and long-term axonal loss in experimental autoimmune encephalomyelitis using Wallerian degeneration slow (WldS) mutant mice. Results: The highest numbers of axons undergoing Wallerian degeneration were found in the perilesional white matter of multiple sclerosis patients early in the disease course and with actively demyelinating lesions. Furthermore, Wallerian degeneration was more abundant in patients harboring chronic active as compared to chronic inactive lesions. No co-localization of neuropeptide Y-Y1 receptor, a bona fide immunohistochemical marker of Wallerian degeneration, with amyloid precursor protein, frequently used as an indicator of acute axonal transport disturbance, was observed in human and mouse tissue, indicating distinct axon-degenerative processes. Experimentally, a delay of Wallerian degeneration, as observed in WldS mice, did not result in a reduction of clinical disability or acute axonal damage in experimental autoimmune encephalomyelitis, further supporting that acute axonal damage as reflected by axonal transport disturbances does not share common molecular mechanisms with Wallerian degeneration. Furthermore, delaying Wallerian degeneration did not result in a net rescue of axons in late lesion stages of experimental autoimmune encephalomyelitis. Conclusions: Our data indicate that in multiple sclerosis, ongoing demyelination in focal lesions is associated with axonal degeneration in the perilesional white matter, supporting a role for focal pathology in diffuse white matter damage. Also, our results suggest that interfering with Wallerian degeneration in inflammatory demyelination does not suffice to prevent acute axonal damage and finally axonal loss."],["dc.identifier.doi","10.1186/s12974-017-0831-8"],["dc.identifier.isi","000397153100002"],["dc.identifier.pmid","28302146"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14381"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Relationship of acute axonal damage, Wallerian degeneration, and clinical disability in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","185"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","190"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Wendling, U."],["dc.contributor.author","Nolte, C."],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:32:35Z"],["dc.date.available","2018-11-07T10:32:35Z"],["dc.date.issued","2002"],["dc.description.abstract","Macrophages/microglia are the key effector cells in myelin removal. Differences exist in the amount and time course of myelin uptake in the central (CNS) and peripheral nervous system (PNS), the basis of this difference, however, is not yet clarified. In the present experiments we studied the phagocytosis rate of CNS or PNS myelin by macrophages and microglia in vitro. Additionally, the effects of intravenous immunoglobulins (IVIg) on this process were investigated. In the PNS experiments, sciatic nerves were cocultured with peritoneal macrophages. Optic nerve fragments were used to characterize the myelin-removing properties of microglia. Cocultures with peritoneal macrophages aimed at investigating the differences in phagocytosis between resident microglia and added macrophages. The myelin phagocytosis in sciatic nerve fragments was higher than in optic nerves, indicating differences in the myelin uptake rate between peripheral macrophages and microglia. IVIg increased the phagocytosis of PNS myelin by macrophages, but not by microglia in optic nerves. The addition of peritoneal macrophages to optic nerve fragments did not lead to an increase in the phagocytosis of CNS myelin either. The IVIg induced phagocytosis of PNS myelin by peripheral macrophages was associated with an increased expression of macrophage Fc receptors measured by FACS. Blocking of Fc receptors by anti-Fc receptor antibody reduced the IVIg induced PNS myelin phagocytosis to basic levels, indicating that the induced but not the basic myelin uptake by macrophages is Fc receptor dependent. In contrast to peripheral macrophages, IVIg did not increase Fc receptor density on microglia. These data indicate that phagocytosis of PNS and CNS myelin by macrophages or microglia is differentially regulated. Local factors within the CNS or PNS may affect this process by modulating the surface receptor profile and activation state of the phagocytic cell or the structure of the myelin sheath. (C) 2002 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jnr.10104"],["dc.identifier.isi","000173099000006"],["dc.identifier.pmid","11782962"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44382"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Differential regulation of myelin phagocytosis by macrophages/microglia, involvement of target myelin, Fc receptors and activation by intravenous immunoglobulins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]