Oligodendrocytes met neurotrophins in the early 1990s of the last century. Since then, their relationship underwent functional ups and downs partially dependent on the developmental stage of the oligodendroglial cells and the species, from which the cells were derived. This review provides a brief overview of oligodendroglial cells and neurotrophins, characterizes neurotrophin signaling during oligodendroglial development, and discusses the significance of proneurotrophins and sortilin for oligodendroglial death and survival. Furthermore, data are provided that TrkA, the tyrosine kinase competent NGF receptor, is localized to caveolincontaining microdomains on the oligodendroglial plasma membrane; an interplay of caveolin and NGF signaling via TrkA might be of functional importance. Finally, experimental evidence of studies is presented which support the idea that neurotrophins are promising candidates for improving oligodendroglial regeneration and remyelination.
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http://dx.doi.org/10.1007/s12031-008-9053-y | DOI Listing |
Int J Mol Sci
December 2024
Institut für Biochemie, Friedrich-Alexander-Universität Erlangen-Nürnberg, D91054 Erlangen, Germany.
Oligodendroglial cells generate myelin sheaths in the vertebrate central nervous system to render rapid saltatory conduction possible and express the highly related Sox8, Sox9 and Sox10 transcription factors. While Sox9 and Sox10 fulfill crucial regulatory roles, Sox8 has only a limited impact on oligodendroglial development and myelination. By replacing Sox10 with Sox8 or Sox9 in the oligodendroglial Oln93 cell line, and comparing the expression profiles, we show here that Sox8 regulates the same processes as Sox10 and Sox9, but exhibits a substantially lower transcriptional activity under standard culture conditions.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Pathology, University of Iowa, Iowa City, IA 52242, USA.
Oligodendroglial lineage cells (OLCs) are critical for neuronal support functions, including myelination and remyelination. Emerging evidence reveals their active roles in neuroinflammation, particularly in conditions like Multiple Sclerosis (MS). This study explores the inflammatory translatome of OLCs during the early onset of experimental autoimmune encephalomyelitis (EAE), an established MS model.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Alzheimer's disease (AD) is a central nervous system degenerative disease with a stealthy onset and a progressive course characterized by memory loss, cognitive dysfunction, and abnormal psychological and behavioral symptoms. However, the pathogenesis of AD remains elusive. An increasing number of studies have shown that oligodendrocyte progenitor cells (OPCs) and oligodendroglial lineage cells (OLGs), especially OPCs and mature oligodendrocytes (OLGs), which are derived from OPCs, play important roles in the pathogenesis of AD.
View Article and Find Full Text PDFNeuroImmune Pharm Ther
September 2024
Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA.
Multiple sclerosis (MS) is a chronic and debilitating autoimmune disease of the central nervous system (CNS) in which a CNS-driven immune response destroys myelin, leading to wide range of symptoms including numbness and tingling, vision problems, mobility impairment, etc. Oligodendrocytes are the myelinating cells in the CNS, which are generated from oligodendroglial progenitor cells (OPCs) via differentiation. However, for multiple reasons, OPCs fail to differentiate to oligodendrocytes in MS and as a result, stimulating the differentiation of OPCs to oligodendrocytes is considered beneficial for MS.
View Article and Find Full Text PDFGlia
December 2024
Molecular and Cellular Pharmacology Program, Stony Brook, New York, USA.
Chronic stress is a major contributor to the development of major depressive disorder, one of the leading causes of disability worldwide. Using a model of repeated social defeat stress in mice, we and others have reported that neuroinflammation plays a dynamic role in the development of behavioral deficits consistent with social avoidance and impaired reward responses. Animals susceptible to the model also exhibit hypomyelination in the medial prefrontal cortex, indicative of changes in the differentiation pathway of cells of the oligodendroglial lineage (OLN).
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