Activation of the subventricular zone in multiple sclerosis: Evidence for early glial progenitors
Brahim Nait-Oumesmar,Nathalie Picard-Riera,Christophe Kerninon,Laurence Decker,Danielle Seilhean,Günter U. Höglinger,Etienne C. Hirsch,Richard Reynolds,Anne Baron-Van Evercooren +8 more
TL;DR: Data indicate that, as in rodents, activation of gliogenesis in the SVZ occurs in MS and suggest the mobilization of SVZ-derived early glial progenitors to periventricular lesions, where they could give rise to oligodendrocyte precursors.
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Abstract: In multiple sclerosis (MS), oligodendrocyte and myelin destruction lead to demyelination with subsequent axonal loss. Experimental demyelination in rodents has highlighted the activation of the subventricular zone (SVZ) and the involvement of progenitor cells expressing the polysialylated form of neural cell adhesion molecule (PSA-NCAM) in the repair process. In this article, we studied the distribution of early PSA-NCAM+ progenitors in the SVZ and MS lesions in human postmortem brains. Compared with controls, MS SVZ showed a 2- to 3-fold increase in cell density and proliferation, which correlated with enhanced numbers of PSA-NCAM+ and glial fibrillary acidic protein-positive (GFAP+) cells. PSA-NCAM+ progenitors mainly were Sox9+, and a few expressed Sox10 and Olig2, markers of oligodendroglial specification. PSA-NCAM+ progenitors expressing Sox10 and Olig2 also were detected in demyelinated MS lesions. In active and chronic active lesions, the number of PSA-NCAM+ progenitors was 8-fold higher compared with chronic silent lesions, shadow plaques, and normal-appearing white matter. In active and chronic active lesions, PSA-NCAM+ progenitors were more frequent in periventricular lesions (30–50%) than in lesions remote from the ventricular wall. These data indicate that, as in rodents, activation of gliogenesis in the SVZ occurs in MS and suggest the mobilization of SVZ-derived early glial progenitors to periventricular lesions, where they could give rise to oligodendrocyte precursors. These early glial progenitors could be a potential target for therapeutic strategies designed to promote myelin repair in MS.
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Citations
Fluvoxamine stimulates oligodendrogenesis of cultured neural stem cells and attenuates inflammation and demyelination in an animal model of multiple sclerosis
Majid Ghareghani,Kazem Zibara,Heibatollah Sadeghi,Shima Dokoohaki,Hossein Sadeghi,Roya Aryanpour,Amir Ghanbari +6 more
TL;DR: Besides its antidepressant activity, fluvoxamine stimulates proliferation and differentiation of NSCs particularly toward oligodendrocytes, a producer of CNS myelin, a new biomarker of MS progression.
Bone Morphogenetic Protein 4 Signalling in Neural Stem and Progenitor Cells during Development and after Injury
TL;DR: Recent studies on BMP4 signalling in the generation of neurons, astrocytes, and oligodendroglial cells in the CNS are reviewed and putative mechanisms that B MP4 may utilise to influence glial cell development following CNS injury are discussed.
Remyelination after chronic spinal cord injury is associated with proliferation of endogenous adult progenitor cells after systemic administration of guanosine
Shucui Jiang,Patrizia Ballerini,Silvana Buccella,Patricia Giuliani,Cai Jiang,Xinjie Huang,Michel P. Rathbone +6 more
TL;DR: It is concluded that functional improvement and remyelination after systemic administration of guanosine is due to the effect of Guanosine/guanine on the proliferation of adult progenitor cells and their maturation into myelin-forming cells.
Olig1 is expressed in human oligodendrocytes during maturation and regeneration.
Ahmad Othman,David M. Frim,Paul E. Polak,Snezana Vujicic,Barry G. W. Arnason,Anne I. Boullerne +5 more
TL;DR: The findings point to different roles of Olig1 and Olig2 in regeneration of cultured adult human oligodendrocytes, Noticeably, the transcriptional profiles found in cultured neonatal rodent OPC are different.
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Inflammation in multiple sclerosis: consequences for remyelination and disease progression
TL;DR: Current knowledge regarding mechanisms of remyelination and remyelination failure in multiple sclerosis and animal models of the disease are summarized, open questions are identified, open questions are identified, challenge existing concepts, and strategies to overcome the translational roadblock in the field of remyelination-promoting therapies are discussed.
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