Disease relevance of Oligodendroglia

• These results support a role for Ptprz in oligodendrocyte survival and in recovery from demyelinating disease [1].
• We further demonstrate that expression of PTPRZ1, the human homolog of Ptprz, is induced in multiple sclerosis lesions and that the gene is specifically expressed in remyelinating oligodendrocytes in these lesions [1].
• Antibodies against Nogo-A stain CNS myelin and oligodendrocytes and allow dorsal root ganglion neurites to grow on CNS myelin and into optic nerve explants [2].
• This antibody binds to a specific cell-surface antigen that is present on C6 rat glioma cells, transformed astrocytes and oligodendrocytes, and a human glioma cell line but is absent on a normal glial cell line, fibroblasts, and primary cultures of astrocytes and oligodendrocytes [3].
• Using rat optic nerve explants, CNS frozen sections, cultured oligodendrocytes or CNS myelin, we show here that highly invasive CNS tumor line (C6 glioblastoma) was not inhibited by these myelin-associated inhibitory components [4].

Psychiatry related information on Oligodendroglia

• Finally, the formation of oligodendrocytes is triggered by an increase in the activity of bHLH factors Olig1 and Olig2 that may be coupled with a decrease in Id activity [5].
• Proteins derived from neurons and oligodendrocytes are found in CA and to understand their origins brain tissue from patients with Alzheimer's disease (AD), multiple sclerosis (MS) and Pick's disease (PD) were tested for complement activity [6].

High impact information on Oligodendroglia

• Recently we have shown that unlike Schwann cells, the process of myelination by oligodendrocyte is independent of Neuregulin1/ErbB signaling [7]
• Here we show that Cnp1, which encodes 2',3'-cyclic nucleotide phosphodiesterase in oligodendrocytes, is essential for axonal survival but not for myelin assembly [8].
• F3/contactin acts as a functional ligand for Notch during oligodendrocyte maturation [9].
• Increasing evidence suggests that, in addition to the inhibitory Jagged1/Notch1 signaling cascade, other pathways act via Notch to mediate oligodendrocyte differentiation [9].
• F3/Notch signaling promotes oligodendrocyte precursor cell differentiation and upregulates the myelin-related protein MAG in OLN-93 cells [9].
• The oligodendrocyte lineage genes Olig1 and Olig2 encode related bHLH proteins that are coexpressed in neural progenitors [10].

Chemical compound and disease context of Oligodendroglia

• Calcium-permeable AMPA/kainate receptors mediate toxicity and preconditioning by oxygen-glucose deprivation in oligodendrocyte precursors [11].
• Peroxynitrite generated by inducible nitric oxide synthase and NADPH oxidase mediates microglial toxicity to oligodendrocytes [12].
• During later stages of Wallerian degeneration, oligodendrocytes express clusterin, a glycoprotein implicated in several conditions of cell degeneration [13].
• Glutamate excitotoxicity is implicated in the progressive loss of oligodendrocytes in multiple sclerosis, but how glutamate metabolism is dysregulated in the disease remains unclear [14].
• Pregnant rats on the 19th day of gestation were given injections with either ethyl nitrosourea (10 micrograms/g body weight) in phosphate-buffered saline or phosphate-buffered saline, and oligodendrocyte cultures were prepared [15].

Biological context of Oligodendroglia

• Rio Hortega coined the term 'oligodendroglia' to define a glial cell population that exhibited few processes in his silver impregnated brain sections. [16]
• Oligodendrocytes are the specialized cells, in the mammalian central nervous system (CNS), which wraps myelin sheath around neuronal processes called as axons [17]
• A single oligodendrocytes can myelinate several axonal segments, the number varying between 1-30 [18]
• Signals derived from astrocytes and neurons (mainly axons) greatly influence differentiation and the precise numbers of oligodendrocytes that are necessary to myelinate the entire CNS [19]
• Several lines of evidence suggest that tyrosine phosphorylation is a key element in myelin formation, differentiation of oligodendrocytes and Schwann cells, and recovery from demyelinating lesions [1].
• Under conditions in which oligodendrocytes inhibit neuronal regeneration, dimerization of IL-2 might provide a mechanism to permit nerve growth [20].
• The results suggest that molecular mimicry between viral core proteins and TAL-H may play a role in breaking immunological tolerance and leading to a selective destruction of oligodendrocytes in MS [21].
• Oligodendrocytes undergoing apoptosis expressed p75, and the absence of p75 resulted in a decrease in the number of apoptotic oligodendrocytes and increased survival of oligodendrocytes [22].
• These findings show that LIF is released by astrocytes in response to ATP liberated from axons firing action potentials, and LIF promotes myelination by mature oligodendrocytes [23].

Anatomical context of Oligodendroglia

• Ptprz encodes protein tyrosine phosphatase receptor type Z (Ptpz, also designated Rptpbeta), which is expressed primarily in the nervous system but also in oligodendrocytes, astrocytes and neurons [1].
• Developing CXCR2 null spinal cords contained reduced oligodendrocytes, abnormally concentrated at the periphery [24].
• By temporally selective interactions with other transcription factors, Olig2 first directs motor neuron fate and later switches to promoting oligodendrocyte production [25].
• Here we show that mature oligodendrocytes in adult animals, as well as astrocytes and microglia, are able to respond to damage in the CNS following trauma by incorporating tritiated thymidine into their nuclei [26].
• Low-affinity AMPA (alpha-amino-3-hydroxy-5-methyl isoxazole propionic acid) and kainate glutamate receptors are also expressed by some glial cells, including oligodendrocyte precursor cells (OPCs) [27].

Associations of Oligodendroglia with chemical compounds

• Since oligodendrocytes express functional alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate-type glutamate receptors, we examined the possibility that oligodendrocyte death can be mediated by glutamate receptor overactivation [28].
• Oligodendrocytes from forebrain are highly vulnerable to AMPA/kainate receptor-mediated excitotoxicity [28].
• In vivo, differentiated oligodendrocytes in subcortical white matter expressed AMPA receptors and were selectively injured by microstereotaxic injection of AMPA but not NMDA [28].
• These results indicate that OPCs are a direct target of interneuronal collaterals and that the GABA-induced Cl(-) flux generated by these events may influence oligodendrocyte development by regulating the efficacy of glutamatergic signaling in OPCs [29].
• Failure of repair correlated with a reduction in the pool of proliferating oligodendrocyte progenitors (bromodeoxyuridine-labeled NG2(+) cells) followed by a reduction in the number of mature oligodendrocytes [30].

Gene context of Oligodendroglia

• In brain, BACE1 mainly colocalizes with RTN3 in neurons, whereas RTN4 is more enriched in oligodendrocytes [31].
• We now report that recombinant human IL-2 influences the growth of glial cells--specifically, the proliferation and differentiation of oligodendrocytes [32].
• In agreement, compound loss of Sox9 and Sox10 led to a further decrease in oligodendrocyte progenitors [33].
• TNF alpha promotes proliferation of oligodendrocyte progenitors and remyelination [30].
• The ventral generation of oligodendrocytes requires Nkx6-regulated expression of the bHLH gene Olig2 in this domain [34].

Analytical, diagnostic and therapeutic context of Oligodendroglia

• Localization of J1-160/180 mRNA by in situ hybridization in the cerebellum, hippocampus and olfactory bulb confirmed the expression of J1-160/180 by oligodendrocytes with a peak of transcription at 7-14 d after birth, indicating a functional role during myelination [35].
• The distributions of the encoded polypeptides were studied by immunofluorescence and confocal microscopy and compared with patterns of MBP expression in normal mouse oligodendrocytes in situ and in culture [36].
• In primary cerebellar cell cultures, N-CAM180 antibody reacts intracellularly with all types of neural cells including astrocytes, oligodendrocytes, and neurons [37].
• Disrupted proteolipid protein trafficking results in oligodendrocyte apoptosis in an animal model of Pelizaeus-Merzbacher disease [38].
• We have studied transport and localization of MBP mRNA in oligodendrocytes in culture by microinjecting labeled mRNA into living cells and analyzing the intracellular distribution of the injected RNA by confocal microscopy [39].

References