Experts and Doctors on oligodendroglia in Germany

Summary

Locale: Germany
Topic: oligodendroglia

Top Publications

  1. Corbeil D, Roper K, Fargeas C, Joester A, Huttner W. Prominin: a story of cholesterol, plasma membrane protrusions and human pathology. Traffic. 2001;2:82-91 pubmed
  2. Kassmann C, Nave K. Oligodendroglial impact on axonal function and survival - a hypothesis. Curr Opin Neurol. 2008;21:235-41 pubmed publisher
    ..Collectively, experimental and pathological findings point to a primary role of myelinating glia in long-term axonal support and suggest that defects of lipid metabolism in oligodendrocytes contribute to inflammatory myelin diseases. ..
  3. Parlapani E, Schmitt A, Erdmann A, Bernstein H, Breunig B, Gruber O, et al. Association between myelin basic protein expression and left entorhinal cortex pre-alpha cell layer disorganization in schizophrenia. Brain Res. 2009;1301:126-34 pubmed publisher
    ..Correlation between reduced MBP as a sign of down-regulated MBP gene expression and disorganization of pre-alpha-cell clusters supports a neurodevelopmental origin of pathological processes in schizophrenia. ..
  4. Kremer D, Göttle P, Hartung H, Küry P. Pushing Forward: Remyelination as the New Frontier in CNS Diseases. Trends Neurosci. 2016;39:246-263 pubmed publisher
    ..Here, we discuss CNS pathologies characterized by white matter degeneration and regeneration and highlight drugs that could potentially serve as remyelination therapies. ..
  5. Hack M, Sugimori M, Lundberg C, Nakafuku M, Gotz M. Regionalization and fate specification in neurospheres: the role of Olig2 and Pax6. Mol Cell Neurosci. 2004;25:664-78 pubmed
    ..Thus, a pathway combining transcription factors of dorsal and ventral regions is activated in the neurosphere culture model. ..
  6. Bernstein H, Lendeckel U, Bertram I, Bukowska A, Kanakis D, Dobrowolny H, et al. Localization of neuregulin-1alpha (heregulin-alpha) and one of its receptors, ErbB-4 tyrosine kinase, in developing and adult human brain. Brain Res Bull. 2006;69:546-59 pubmed
    ..Our data show that NRG-1alpha expression is lower in the adult human brain than in the developing brain, and, therefore, support a role for NRG-1alpha in brain development. ..
  7. Fitzner D, Schnaars M, van Rossum D, Krishnamoorthy G, Dibaj P, Bakhti M, et al. Selective transfer of exosomes from oligodendrocytes to microglia by macropinocytosis. J Cell Sci. 2011;124:447-58 pubmed publisher
    ..By designating the capacity for macropinocytosis and antigen presentation to distinct cells, degradation and immune function might be assigned to different subtypes of microglia. ..
  8. Richter Landsberg C, Heinrich M. OLN-93: a new permanent oligodendroglia cell line derived from primary rat brain glial cultures. J Neurosci Res. 1996;45:161-73 pubmed
  9. Kuhlmann T, Miron V, Cui Q, Cuo Q, Wegner C, Antel J, et al. Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. Brain. 2008;131:1749-58 pubmed publisher
    ..In summary, we provide evidence that a differentiation block of oligodendroglial progenitors is a major determinant of remyelination failure in chronic multiple sclerosis lesions. ..

More Information

Publications101 found, 100 shown here

  1. Jadasz J, Kremer D, Göttle P, Tzekova N, Domke J, Rivera F, et al. Mesenchymal stem cell conditioning promotes rat oligodendroglial cell maturation. PLoS ONE. 2013;8:e71814 pubmed publisher
    ..We thus conclude that apart from their suggested application as potential anti-inflammatory and immunomodulatory MS treatment, these cells might also be exploited to support endogenous myelin repair activities. ..
  2. Murin R, Verleysdonk S, Rapp M, Hamprecht B. Immunocytochemical localization of 3-methylcrotonyl-CoA carboxylase in cultured ependymal, microglial and oligodendroglial cells. J Neurochem. 2006;97:1393-402 pubmed
    ..The ubiquitous expression of MCC in glial cells demonstrates the ability of the cells to engage in the catabolism of leucine transported into the brain, mainly for the generation of energy. ..
  3. Heidemann A, Schipke C, Kettenmann H. Extracellular application of nicotinic acid adenine dinucleotide phosphate induces Ca2+ signaling in astrocytes in situ. J Biol Chem. 2005;280:35630-40 pubmed
    ..Moreover, NAADP+ triggered responses in all other cell types (cultured cerebellar neurons, microglia, and oligodendrocytes) of the central nervous system. ..
  4. Angelov D, Walther M, Streppel M, Guntinas Lichius O, Van Dam A, Stennert E, et al. ED2-positive perivascular phagocytes produce interleukin-1beta during delayed neuronal loss in the facial nucleus of the rat. J Neurosci Res. 1998;54:820-7 pubmed
    ..We concluded that, during delayed neuronal death "behind" an intact blood-brain barrier, the perivascular phagocytes were more likely to function as antigen-presenting cells than the parenchymal microglia. ..
  5. Tulpule K, Schmidt M, Boecker K, Goldbaum O, Richter Landsberg C, Dringen R. Formaldehyde induces rapid glutathione export from viable oligodendroglial OLN-93 cells. Neurochem Int. 2012;61:1302-13 pubmed publisher
    ..The rapid export of GSH from formaldehyde-treated viable oligodendroglial cells is likely to compromise the cellular antioxidative and detoxification potential which may contribute to the known neurotoxicity of formaldehyde. ..
  6. Hennen E, Safina D, Haussmann U, Wörsdörfer P, Edenhofer F, Poetsch A, et al. A LewisX glycoprotein screen identifies the low density lipoprotein receptor-related protein 1 (LRP1) as a modulator of oligodendrogenesis in mice. J Biol Chem. 2013;288:16538-45 pubmed publisher
    ..Here, we provide first evidence that LRP1 is necessary for the differentiation of neural stem cells toward oligodendrocytes. However, this function is independent of LeX glycosylation. ..
  7. Schuster N, Bender H, Philippi A, Subramaniam S, Strelau J, Wang Z, et al. TGF-beta induces cell death in the oligodendroglial cell line OLI-neu. Glia. 2002;40:95-108 pubmed
  8. Sobottka B, Harrer M, Ziegler U, Fischer K, Wiendl H, Hunig T, et al. Collateral bystander damage by myelin-directed CD8+ T cells causes axonal loss. Am J Pathol. 2009;175:1160-6 pubmed publisher
  9. Bakhti M, Winter C, Simons M. Inhibition of myelin membrane sheath formation by oligodendrocyte-derived exosome-like vesicles. J Biol Chem. 2011;286:787-96 pubmed publisher
    ..We propose that neurons control the secretion of autoinhibitory oligodendroglial-derived exosomes to coordinate myelin membrane biogenesis. ..
  10. Boison D, Bussow H, D Urso D, Muller H, Stoffel W. Adhesive properties of proteolipid protein are responsible for the compaction of CNS myelin sheaths. J Neurosci. 1995;15:5502-13 pubmed
    ..We propose that adhesion properties of the extracellular domains of PLP are responsible for the tight apposition of the plasma membrane processes of oligodendrocytes wrapping axons to form the compact myelin sheath. ..
  11. Kunzelmann P, Blumcke I, Traub O, Dermietzel R, Willecke K. Coexpression of connexin45 and -32 in oligodendrocytes of rat brain. J Neurocytol. 1997;26:17-22 pubmed
    ..Expression of connexin45 in oligodendrocytes may prevent dysmyelinating effects of connexin32 mutations in the central nervous system of Charcot-Marie-Tooth (X-type) patients. ..
  12. May D, Tress O, Seifert G, Willecke K. Connexin47 protein phosphorylation and stability in oligodendrocytes depend on expression of Connexin43 protein in astrocytes. J Neurosci. 2013;33:7985-96 pubmed publisher
    ..These results further unravel the complexity of panglial networks and show that results of previous studies using astrocytic Cx43-deficient mice have to be reconsidered. ..
  13. Göbel K, Melzer N, Herrmann A, Schuhmann M, Bittner S, Ip C, et al. Collateral neuronal apoptosis in CNS gray matter during an oligodendrocyte-directed CD8(+) T cell attack. Glia. 2010;58:469-80 pubmed publisher
    ..Collateral neuronal apoptosis could contribute to substantial neuronal loss in gray matter lesions and cause persistent neurological impairment in both acute and chronic gray matter lesions in various inflammatory CNS disorders. ..
  14. Kuhlbrodt K, Herbarth B, Sock E, Enderich J, Hermans Borgmeyer I, Wegner M. Cooperative function of POU proteins and SOX proteins in glial cells. J Biol Chem. 1998;273:16050-7 pubmed
    ..Our data suggest the existence of a specific code in which POU proteins require specific Sox proteins to exhibit cooperative effects in glial cells. ..
  15. Leder C, Schwab N, Ip C, Kroner A, Nave K, Dornmair K, et al. Clonal expansions of pathogenic CD8+ effector cells in the CNS of myelin mutant mice. Mol Cell Neurosci. 2007;36:416-24 pubmed
    ..The association of primary oligodendrocyte damage with secondary expansions of pathogenic cells underlines the role of adaptive immune reactions in neurodegenerative and neuroinflammatory diseases. ..
  16. Mann S, Versmold B, Marx R, Stahlhofen S, Dietzel I, Heumann R, et al. Corticosteroids reverse cytokine-induced block of survival and differentiation of oligodendrocyte progenitor cells from rats. J Neuroinflammation. 2008;5:39 pubmed publisher
  17. Dhaunchak A, Colman D, Nave K. Misalignment of PLP/DM20 transmembrane domains determines protein misfolding in Pelizaeus-Merzbacher disease. J Neurosci. 2011;31:14961-71 pubmed publisher
    ..We conclude that an important determinant in the quality control of polytopic membrane proteins is the free alignment of their TM domains. ..
  18. Kipp M, Victor M, Martino G, Franklin R. Endogeneous remyelination: findings in human studies. CNS Neurol Disord Drug Targets. 2012;11:598-609 pubmed
    ..This comprehensive overview is complemented by recent findings suggesting that U.S. Food and Drug Administration-approved treatment options, such as FTY720 (Gilenya®) or glatiramer acetate (Copaxone®) might boost myelin repair. ..
  19. Theis M, Giaume C. Connexin-based intercellular communication and astrocyte heterogeneity. Brain Res. 2012;1487:88-98 pubmed publisher
    ..This article is part of a Special Issue entitled Electrical Synapses. ..
  20. Imbschweiler I, Seehusen F, Peck C, Omar M, Baumgartner W, Wewetzer K. Increased p75 neurotrophin receptor expression in the canine distemper virus model of multiple sclerosis identifies aldynoglial Schwann cells that emerge in response to axonal damage. Glia. 2012;60:358-71 pubmed publisher
    ..Further studies have to address the role of microglia during this process and the regenerative potential of aldynoglial cells in CDV infection and other demyelinating diseases. ..
  21. Göbel K, Bittner S, Melzer N, Pankratz S, Dreykluft A, Schuhmann M, et al. CD4(+) CD25(+) FoxP3(+) regulatory T cells suppress cytotoxicity of CD8(+) effector T cells: implications for their capacity to limit inflammatory central nervous system damage at the parenchymal level. J Neuroinflammation. 2012;9:41 pubmed publisher
    ..Our results suggest that CD4(+) T reg cells are capable of suppressing CD8(+) T effector cell responses at the parenchymal site, that is, limiting parenchymal damage in autoimmune central nervous system inflammation. ..
  22. Tomas Roig J, Wirths O, Salinas Riester G, Havemann Reinecke U. The Cannabinoid CB1/CB2 Agonist WIN55212.2 Promotes Oligodendrocyte Differentiation In Vitro and Neuroprotection During the Cuprizone-Induced Central Nervous System Demyelination. CNS Neurosci Ther. 2016;22:387-95 pubmed publisher
    ..The cannabinoid agonist WIN55212.2 promotes oligodendrocyte differentiation in vitro. Moreover, 0.5 mg/kg of the drug confers neuroprotection during cuprizone-induced demyelination, while 1 mg/kg aggravates the demyelination process. ..
  23. Gerstner B, Gratopp A, Marcinkowski M, Sifringer M, Obladen M, Buhrer C. Glutaric acid and its metabolites cause apoptosis in immature oligodendrocytes: a novel mechanism of white matter degeneration in glutaryl-CoA dehydrogenase deficiency. Pediatr Res. 2005;57:771-6 pubmed
    ..GA, GC, and 3-OH-GA directly initiate the apoptotic cascade in oligodendroglia cells. This mechanism may contribute to the white matter damage observed in glutaryl-CoA dehydrogenase deficiency. ..
  24. Schuster N, Bender H, Rössler O, Philippi A, Dünker N, Thiel G, et al. Transforming growth factor-beta and tumor necrosis factor-alpha cooperate to induce apoptosis in the oligodendroglial cell line OLI-neu. J Neurosci Res. 2003;73:324-33 pubmed
    ..Therefore, we conclude that TNF-alpha and TGF-beta affect partially common pathways but also regulate different steps in the apoptotic cascade. ..
  25. Finzsch M, Stolt C, Lommes P, Wegner M. Sox9 and Sox10 influence survival and migration of oligodendrocyte precursors in the spinal cord by regulating PDGF receptor alpha expression. Development. 2008;135:637-46 pubmed publisher
    ..We thus conclude that Sox9 and Sox10 are required in a functionally redundant manner in oligodendrocyte precursors for PDGF-dependent survival and migration. ..
  26. Cossais F, Sock E, Hornig J, Schreiner S, Kellerer S, Bösl M, et al. Replacement of mouse Sox10 by the Drosophila ortholog Sox100B provides evidence for co-option of SoxE proteins into vertebrate-specific gene-regulatory networks through altered expression. Dev Biol. 2010;341:267-81 pubmed publisher
  27. Knipper M, Bandtlow C, Gestwa L, Köpschall I, Rohbock K, Wiechers B, et al. Thyroid hormone affects Schwann cell and oligodendrocyte gene expression at the glial transition zone of the VIIIth nerve prior to cochlea function. Development. 1998;125:3709-18 pubmed
    ..The thyroid hormone-dependent commencement of nerve conduction is discussed in connection with the patterning refinement of central auditory pathways and the acquisition of deafness. ..
  28. Budde H, Schmitt S, Fitzner D, Opitz L, Salinas Riester G, Simons M. Control of oligodendroglial cell number by the miR-17-92 cluster. Development. 2010;137:2127-32 pubmed publisher
    ..Together, these results suggest that the miRNA pathway is essential in determining oligodendroglial cell number and that the miR-17-92 cluster is crucial in this process. ..
  29. Raasch J, Zeller N, Van Loo G, Merkler D, Mildner A, Erny D, et al. IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous system. Brain. 2011;134:1184-98 pubmed publisher
    ..Thus, therapies targeting I?B kinase 2 function in non-neuronal cells may represent a promising strategy for the treatment of distinct demyelinating central nervous system diseases. ..
  30. BINDER E, Rukavina M, Hassani H, Weber M, Nakatani H, Reiff T, et al. Peripheral nervous system progenitors can be reprogrammed to produce myelinating oligodendrocytes and repair brain lesions. J Neurosci. 2011;31:6379-91 pubmed publisher
    ..These results demonstrate a reprogramming of PNS progenitors to CNS fates without genetic modification and imply that PNS cells could be a potential source for cell-based CNS therapy. ..
  31. Kuhlbrodt K, Herbarth B, Sock E, Hermans Borgmeyer I, Wegner M. Sox10, a novel transcriptional modulator in glial cells. J Neurosci. 1998;18:237-50 pubmed
    ..We propose a role for Sox10 in conferring cell specificity to the function of other transcription factors in developing and mature glia. ..
  32. Angelov D, Arnhold S, Andressen C, Grabsch H, Puschmann M, Hescheler J, et al. Temporospatial relationships between macroglia and microglia during in vitro differentiation of murine stem cells. Dev Neurosci. 1998;20:42-51 pubmed
  33. Niehaus A, Shi J, Grzenkowski M, Diers Fenger M, Archelos J, Hartung H, et al. Patients with active relapsing-remitting multiple sclerosis synthesize antibodies recognizing oligodendrocyte progenitor cell surface protein: implications for remyelination. Ann Neurol. 2000;48:362-71 pubmed
    ..This is the first report describing antibodies in MS against a progenitor cell-specific antigen that may contribute to the development and progression of chronically demyelinated lesions. ..
  34. Werner H, Dimou L, Klugmann M, Pfeiffer S, Nave K. Multiple splice isoforms of proteolipid M6B in neurons and oligodendrocytes. Mol Cell Neurosci. 2001;18:593-605 pubmed
    ..Cotransfection experiments suggest a physical interaction of M6B and mutant PLP, when retained in the endoplasmic reticulum, that may also contribute to oligodendrocyte dysfunction in Pelizaeus-Merzbacher disease. ..
  35. Odermatt B, Wellershaus K, Wallraff A, Seifert G, Degen J, Euwens C, et al. Connexin 47 (Cx47)-deficient mice with enhanced green fluorescent protein reporter gene reveal predominant oligodendrocytic expression of Cx47 and display vacuolized myelin in the CNS. J Neurosci. 2003;23:4549-59 pubmed
    ..The central white matter of these double-deficient mice exhibited much more abundant vacuolation in nerve fibers than mice deficient only in Cx47. ..
  36. Stolt C, Lommes P, Friedrich R, Wegner M. Transcription factors Sox8 and Sox10 perform non-equivalent roles during oligodendrocyte development despite functional redundancy. Development. 2004;131:2349-58 pubmed
    ..Resulting differences in protein amounts might be a main reason for the weaker impact of Sox8 on oligodendrocyte development and for unidirectional compensation of the Sox8 loss by Sox10. ..
  37. Mann S, Meyer J, Dietzel I. Integration of a scanning ion conductance microscope into phase contrast optics and its application to the quantification of morphological parameters of selected cells. J Microsc. 2006;224:152-7 pubmed
    ..We show an application in which surfaces and volumes of somata and processes of cultured cells from the central nervous system were quantified separately. ..
  38. Kassmann C, Lappe Siefke C, Baes M, Brugger B, Mildner A, Werner H, et al. Axonal loss and neuroinflammation caused by peroxisome-deficient oligodendrocytes. Nat Genet. 2007;39:969-76 pubmed
    ..We conclude that peroxisomes provide oligodendrocytes with an essential neuroprotective function against axon degeneration and neuroinflammation, which is relevant for human demyelinating diseases. ..
  39. Murin R, Cesar M, Kowtharapu B, Verleysdonk S, Hamprecht B. Expression of pyruvate carboxylase in cultured oligodendroglial, microglial and ependymal cells. Neurochem Res. 2009;34:480-9 pubmed publisher
  40. Kroner A, Schwab N, Ip C, Leder C, Nave K, Maurer M, et al. PD-1 regulates neural damage in oligodendroglia-induced inflammation. PLoS ONE. 2009;4:e4405 pubmed publisher
    ..Our finding may have implications for understanding the mechanisms leading to the high clinical variability of polygenic or even monogenic disorders of the nervous system. ..
  41. Schmitz M, Klöppner S, Klopfleisch S, Mobius W, Schwartz P, Zerr I, et al. Mutual effects of caveolin and nerve growth factor signaling in pig oligodendrocytes. J Neurosci Res. 2010;88:572-88 pubmed publisher
    ..Subsequently, increased oligodendroglial process formation via NGF was impaired. The present study indicates that CCRs/caveolin could play a modulating role during oligodendroglial differentiation and regeneration. ..
  42. Hoffmann S, Hos D, Küspert M, Lang R, Lovell Badge R, Wegner M, et al. Stem cell factor Sox2 and its close relative Sox3 have differentiation functions in oligodendrocytes. Development. 2014;141:39-50 pubmed publisher
    ..This study presents one of the few cases in which SoxB1 proteins, including the stem cell factor Sox2, are associated with differentiation rather than precursor functions. ..
  43. Jung M, Sommer I, Schachner M, Nave K. Monoclonal antibody O10 defines a conformationally sensitive cell-surface epitope of proteolipid protein (PLP): evidence that PLP misfolding underlies dysmyelination in mutant mice. J Neurosci. 1996;16:7920-9 pubmed
    ..We propose that the O10 epitope emerges as the full length protein reaches a functional tertiary structure and that the absence of this epitope marks a structural defect of PLP that leads to dysmyelination. ..
  44. Bosio A, Binczek E, Haupt W, Stoffel W. Composition and biophysical properties of myelin lipid define the neurological defects in galactocerebroside- and sulfatide-deficient mice. J Neurochem. 1998;70:308-15 pubmed
    ..The loss of the two glycosphingolipid classes causes the breakdown of saltatory conductance of myelinated axons in the cgt-/- mouse. ..
  45. Buch T, Heppner F, Tertilt C, Heinen T, Kremer M, Wunderlich F, et al. A Cre-inducible diphtheria toxin receptor mediates cell lineage ablation after toxin administration. Nat Methods. 2005;2:419-26 pubmed
    ..Notably, we show that the developing DT-specific antibody response is weak and not neutralizing, and thus does not impede the efficacy of DT. Our results validate the use of iDTR mice as a tool for cell ablation in vivo. ..
  46. Wang Z, Spittau B, Behrendt M, Peters B, Krieglstein K. Human TIEG2/KLF11 induces oligodendroglial cell death by downregulation of Bcl-XL expression. J Neural Transm (Vienna). 2007;114:867-75 pubmed
    ..These data suggest that TIEG2 serves as a downstream mediator of TGF-beta, bridging TGF-beta-dependent signaling to the intracellular pathway of apoptosis. ..
  47. Stahnke T, Stadelmann C, Netzler A, Bruck W, Richter Landsberg C. Differential upregulation of heme oxygenase-1 (HSP32) in glial cells after oxidative stress and in demyelinating disorders. J Mol Neurosci. 2007;32:25-37 pubmed
    ..The data suggest that stress-induced HO-1 initially plays a protective role, while its chronic upregulation, might contribute to oligodendroglial cell death rather than providing protection. ..
  48. Nawaz S, Kippert A, Saab A, Werner H, Lang T, Nave K, et al. Phosphatidylinositol 4,5-bisphosphate-dependent interaction of myelin basic protein with the plasma membrane in oligodendroglial cells and its rapid perturbation by elevated calcium. J Neurosci. 2009;29:4794-807 pubmed publisher
    ..Together, these results establish that PIP2 is an essential determinant for stable membrane binding of MBP and provide a novel link between glial phosphoinositol metabolism and MBP function in development and disease. ..
  49. Kroner A, Schwab N, Ip C, Ortler S, Göbel K, Nave K, et al. Accelerated course of experimental autoimmune encephalomyelitis in PD-1-deficient central nervous system myelin mutants. Am J Pathol. 2009;174:2290-9 pubmed publisher
  50. Grimm I, Messemer N, Stanke M, Gachet C, Zimmermann H. Coordinate pathways for nucleotide and EGF signaling in cultured adult neural progenitor cells. J Cell Sci. 2009;122:2524-33 pubmed publisher
  51. Lin J, Luo J, Redies C. Cadherin-19 expression is restricted to myelin-forming cells in the chicken embryo. Neuroscience. 2010;165:168-78 pubmed publisher
    ..Despite their close genetic relation, the three cadherins have acquired functions in rather different cell types during nervous system development. ..
  52. Strauss K, Goebel C, Runz H, Mobius W, Weiss S, Feussner I, et al. Exosome secretion ameliorates lysosomal storage of cholesterol in Niemann-Pick type C disease. J Biol Chem. 2010;285:26279-88 pubmed publisher
    ..Furthermore, we suggest that secretion of cholesterol by exosomes contributes to maintain cellular cholesterol homeostasis. ..
  53. Rena Hesse A, Hagemeier K, Lürbke A, Held J, Friedman H, Peterson A, et al. XIAP protects oligodendrocytes against cell death in vitro but has no functional role in toxic demyelination. Glia. 2012;60:271-80 pubmed publisher
    ..However, lack of XIAP does not modulate oligodendroglial cell death in toxic demyelination in vivo. ..
  54. Kipp M, Amor S. FTY720 on the way from the base camp to the summit of the mountain: relevance for remyelination. Mult Scler. 2012;18:258-63 pubmed publisher
    ..While the mechanisms of action still require firm elucidation, it is clear that FTY720 could also be reparative, extending its therapeutic potential for multiple sclerosis...
  55. Binamé F, Sakry D, Dimou L, Jolivel V, Trotter J. NG2 regulates directional migration of oligodendrocyte precursor cells via Rho GTPases and polarity complex proteins. J Neurosci. 2013;33:10858-74 pubmed publisher
    ..This work also reveals CRB and PAR polarity complexes as new effectors of NG2 signaling in the establishment of front-rear polarity. ..
  56. Stone S, Jamison S, Yue Y, Durose W, Schmidt Ullrich R, Lin W. NF-κB Activation Protects Oligodendrocytes against Inflammation. J Neurosci. 2017;37:9332-9344 pubmed publisher
    ..The results presented in this study represent the first demonstration that NF-κB activation acts cell autonomously to protect oligodendrocytes against inflammation in animal models of MS. ..
  57. Schreiber J, Enderich J, Sock E, Schmidt C, Richter Landsberg C, Wegner M. Redundancy of class III POU proteins in the oligodendrocyte lineage. J Biol Chem. 1997;272:32286-93 pubmed
    ..Taken together, our data imply a partial, but not complete redundancy between POU proteins in oligodendrocytes. ..
  58. Ankerhold R, Leppert C, Bastmeyer M, Stuermer C. E587 antigen is upregulated by goldfish oligodendrocytes after optic nerve lesion and supports retinal axon regeneration. Glia. 1998;23:257-70 pubmed
  59. Jaszai J, Farkas L, Galter D, Reuss B, Strelau J, Unsicker K, et al. GDNF-related factor persephin is widely distributed throughout the nervous system. J Neurosci Res. 1998;53:494-501 pubmed
    ..We conclude that PSP is synthesized throughout the nervous system and that it is presumably of both astroglial and neuronal origin, in contrast to GDNF and neurturin, which seem to be predominantly of neuronal origin. ..
  60. Spörkel O, Uschkureit T, Bussow H, Stoffel W. Oligodendrocytes expressing exclusively the DM20 isoform of the proteolipid protein gene: myelination and development. Glia. 2002;37:19-30 pubmed
  61. Davidoff M, Middendorff R, Köfüncü E, Muller D, Jezek D, Holstein A. Leydig cells of the human testis possess astrocyte and oligodendrocyte marker molecules. Acta Histochem. 2002;104:39-49 pubmed
    ..Furthermore, the established immunohistochemical similarities are consistent with the assumption that foetal and postnatal Leydig cells are of common origin. ..
  62. Saher G, Brugger B, Lappe Siefke C, Mobius W, Tozawa R, Wehr M, et al. High cholesterol level is essential for myelin membrane growth. Nat Neurosci. 2005;8:468-75 pubmed
    ..This shows that cholesterol is an indispensable component of myelin membranes and that cholesterol availability in oligodendrocytes is a rate-limiting factor for brain maturation. ..
  63. Ip C, Kroner A, Bendszus M, Leder C, Kobsar I, Fischer S, et al. Immune cells contribute to myelin degeneration and axonopathic changes in mice overexpressing proteolipid protein in oligodendrocytes. J Neurosci. 2006;26:8206-16 pubmed
    ..These findings provide strong evidence that a primary glial damage can cause secondary immune reactions of pathological significance as it has been suggested for some forms of multiple sclerosis and other leukodystrophies. ..
  64. Stolt C, Schlierf A, Lommes P, Hillgärtner S, Werner T, Kosian T, et al. SoxD proteins influence multiple stages of oligodendrocyte development and modulate SoxE protein function. Dev Cell. 2006;11:697-709 pubmed
    ..Our studies reveal a complex regulatory network between different groups of Sox proteins that is essential for proper progression of oligodendrocyte development. ..
  65. Schweitzer J, Gimnopoulos D, Lieberoth B, Pogoda H, Feldner J, Ebert A, et al. Contactin1a expression is associated with oligodendrocyte differentiation and axonal regeneration in the central nervous system of zebrafish. Mol Cell Neurosci. 2007;35:194-207 pubmed
    ..These complex regulation patterns suggest roles for Cntn1a in myelinating cells and neurons particularly in successful CNS regeneration. ..
  66. Buss A, Pech K, Kakulas B, Martin D, Schoenen J, Noth J, et al. NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury. BMC Neurol. 2009;9:32 pubmed publisher
    ..The present data points to the importance of such correlative investigations for demonstrating the clinical relevance of experimental data. ..
  67. Rönicke S, Kruska N, Kahlert S, Reiser G. The influence of the branched-chain fatty acids pristanic acid and Refsum disease-associated phytanic acid on mitochondrial functions and calcium regulation of hippocampal neurons, astrocytes, and oligodendrocytes. Neurobiol Dis. 2009;36:401-10 pubmed publisher
    ..In conclusion, pristanic acid as well as phytanic acid induced a complex array of toxic activities with mitochondrial dysfunction and Ca2+ deregulation...
  68. Happel P, Möller K, Kunz R, Dietzel I. A boundary delimitation algorithm to approximate cell soma volumes of bipolar cells from topographical data obtained by scanning probe microscopy. BMC Bioinformatics. 2010;11:323 pubmed publisher
    ..We provide a new algorithm to repeatedly determine single cell soma volume and thus to quantify cell volume changes during cell movements occuring over a time range of hours. ..
  69. Czopka T, von Holst A, Ffrench Constant C, Faissner A. Regulatory mechanisms that mediate tenascin C-dependent inhibition of oligodendrocyte precursor differentiation. J Neurosci. 2010;30:12310-22 pubmed publisher
    ..Our study therefore uncovers the first signaling pathways that underlie Tnc-induced, ECM-dependent maintenance of the immature state of OPCs. ..
  70. Hagemeier K, Lürbke A, Hucke S, Albrecht S, Preisner A, Klassen E, et al. Puma, but not noxa is essential for oligodendroglial cell death. Glia. 2013;61:1712-23 pubmed publisher
    ..Our data demonstrate that Puma is pivotal for oligodendroglial cell death induced by different cell death stimuli and might play a role in oligodendroglial cell death in MS. ..
  71. Lappe Siefke C, Goebbels S, Gravel M, Nicksch E, Lee J, Braun P, et al. Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination. Nat Genet. 2003;33:366-74 pubmed
    ..Oligodendrocyte dysfunction, such as that in multiple sclerosis lesions, may suffice to cause secondary axonal loss. ..
  72. Happel P, Hoffmann G, Mann S, Dietzel I. Monitoring cell movements and volume changes with pulse-mode scanning ion conductance microscopy. J Microsc. 2003;212:144-51 pubmed
    ..Difference images indicate that volume changes can affect cell surfaces inhomogeneously, emphasizing the role of the cytoskeleton in the stabilization of cell shape. ..
  73. Hövelmeyer N, Hao Z, Kranidioti K, Kassiotis G, Buch T, Frommer F, et al. Apoptosis of oligodendrocytes via Fas and TNF-R1 is a key event in the induction of experimental autoimmune encephalomyelitis. J Immunol. 2005;175:5875-84 pubmed
    ..Although only moderate reduction of lymphocyte infiltration into CNS tissue was observed, the absence of these receptors appears to confer protection from demyelination and development of clinical disease. ..
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