Oligodendroglial Epigenetics, from Lineage Specification to Activity-Dependent Myelination

Pruvost, Mathilde; Moyon, Sarah

doi:10.3390/life11010062

Cited by 13 publications

(11 citation statements)

References 244 publications

(334 reference statements)

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“…On the other hand, the MAG analysis showed similar data to MOG. At 2 WPI, the group administered with EGF–GNPs showed an increase in MAG, compared to the Ctrl and CPZ groups, which suggest that an early remyelination is ongoing [ 34 , 35 , 36 ]. At 3 WPI, the increase in MAG was more evident in the EGF–GNPs group with respect to the CPZ and EGF groups, indicating that soluble EGF (not coupled with GNPs) is less effective in promoting myelin protein synthesis than the EGF coupled with GNPs.…”

Section: Discussionmentioning

confidence: 99%

EGF-Coupled Gold Nanoparticles Increase the Expression of CNPase and the Myelin-Associated Proteins MAG, MOG, and MBP in the Septal Nucleus Demyelinated by Cuprizone

Lira-Diaz

Monroy-Rodriguez

González-Pedroza

et al. 2022

Life

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Current pharmacological therapies against demyelinating diseases are not quite satisfactory to promote remyelination. Epidermal growth factor (EGF) can expand the population of oligodendrocyte precursor cells (OPCs) that may help with the remyelination process, but its delivery into the injured tissue is still a biomedical challenge. Gold nanoparticles (GNPs) may be a useful tool for drug delivery into the brain. To evaluate remyelination in the septal nucleus, we administered intracerebral GNPs coupled with EGF (EGF–GNPs). C57BL6/J mice were demyelinated with 0.4% cuprizone (CPZ) and divided into several groups: Sham, Ctrl, GNPs, EGF, and EGF–GNPs. We evaluated the remyelination process at two time-points: 2 weeks and 3 weeks post-injection (WPI) of each treatment. We used the rotarod for evaluating motor coordination. Then, we did a Western blot analysis myelin-associated proteins: CNPase, MAG, MOG, and MBP. EGF–GNPs increase the expression of CNPase, MAG, and MOG at 2 WPI. At 3 WPI, we found that the EGF–GNPs treatment improves motor coordination and increases MAG, MOG, and MBP. EGF–GNPs enhance the expression of myelin-associated proteins and improve the motor coordination in mice. Thus, EGF-associated GNPs may be a promising pharmacological vehicle for delivering long-lasting drugs into the brain.

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Section: Discussionmentioning

confidence: 99%

EGF-Coupled Gold Nanoparticles Increase the Expression of CNPase and the Myelin-Associated Proteins MAG, MOG, and MBP in the Septal Nucleus Demyelinated by Cuprizone

Lira-Diaz

Monroy-Rodriguez

González-Pedroza

et al. 2022

Life

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“…Oligodendrocytes and their progenitors are directly involved in membrane and metabolic interactions with neurons during the different phases of destruction and regeneration of the myelin sheath, driven by the dynamic and fluctuating expression of many transcription factors [ 179 ]. The activity of the nervous system is intimately linked to the epigenetic regulation of the activity of these factors and to the neo-expression of certain genes involved in the functional dynamics of the production/destruction of myelin [ 158 ]. Correct myelination is essential for the proper development and evolution of neuronal connections and the adaptation of brain function to the environment.…”

Section: Potential Involvements Of Epigenetic Mechanisms In Myelin Re...mentioning

confidence: 99%

Myelin in Alzheimer’s disease: culprit or bystander?

Maître

Jeltsch-David

Okechukwu

et al. 2023

acta neuropathol commun

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Alzheimer’s disease (AD) is a neurodegenerative disorder with neuronal and synaptic losses due to the accumulation of toxic amyloid β (Αβ) peptide oligomers, plaques, and tangles containing tau (tubulin-associated unit) protein. While familial AD is caused by specific mutations, the sporadic disease is more common and appears to result from a complex chronic brain neuroinflammation with mitochondriopathies, inducing free radicals’ accumulation. In aged brain, mutations in DNA and several unfolded proteins participate in a chronic amyloidosis response with a toxic effect on myelin sheath and axons, leading to cognitive deficits and dementia. Αβ peptides are the most frequent form of toxic amyloid oligomers. Accumulations of misfolded proteins during several years alters different metabolic mechanisms, induce chronic inflammatory and immune responses with toxic consequences on neuronal cells. Myelin composition and architecture may appear to be an early target for the toxic activity of Aβ peptides and others hydrophobic misfolded proteins. In this work, we describe the possible role of early myelin alterations in the genesis of neuronal alterations and the onset of symptomatology. We propose that some pathophysiological and clinical forms of the disease may arise from structural and metabolic disorders in the processes of myelination/demyelination of brain regions where the accumulation of non-functional toxic proteins is important. In these forms, the primacy of the deleterious role of amyloid peptides would be a matter of questioning and the initiating role of neuropathology would be primarily the fact of dysmyelination.

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“…Neuron–OPC synapses may be the important contact points between the two cell types which give neurons a possibility to regulate proliferation and differentiation of OPCs, as well as myelination, in an activity-dependent fashion. There is, indeed, clear evidence that neuronal activity modulates behaviour of OPCs and myelination [ 46 , 47 ]. Furthermore, neuronal modulation of OPCs’ behaviour is not an all-or-none signal, but may depend on the firing pattern of neurons, i.e., some patterns of neuronal activity are more likely to promote proliferation of OPCs while others are more likely to promote their differentiation [ 12 ].…”

Section: Temporal Aspects Of Ampar-mediated Signalling In Ol Lineage ...mentioning

confidence: 99%

Recent Insights into the Functional Role of AMPA Receptors in the Oligodendrocyte Lineage Cells In Vivo

Kukley

2023

IJMS

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This review discusses the experimental findings of several recent studies which investigated the functional role of AMPA receptors (AMPARs) in oligodendrocyte lineage cells in vivo, in mice and in zebrafish. These studies provided valuable information showing that oligodendroglial AMPARs may be involved in the modulation of proliferation, differentiation, and migration of oligodendroglial progenitors, as well as survival of myelinating oligodendrocytes during physiological conditions in vivo. They also suggested that targeting the subunit composition of AMPARs may be an important strategy for treating diseases. However, at the same time, the experimental findings taken together still do not provide a clear picture on the topic. Hence, new ideas and new experimental designs are required for understanding the functional role of AMPARs in the oligodendrocyte lineage cells in vivo. It is also necessary to consider more closely the temporal and spatial aspects of AMPAR-mediated signalling in the oligodendrocyte lineage cells. These two important aspects are routinely discussed by neuronal physiologists studying glutamatergic synaptic transmission, but are rarely debated and thought about by researchers studying glial cells.

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Oligodendroglial Epigenetics, from Lineage Specification to Activity-Dependent Myelination

Cited by 13 publications

References 244 publications

EGF-Coupled Gold Nanoparticles Increase the Expression of CNPase and the Myelin-Associated Proteins MAG, MOG, and MBP in the Septal Nucleus Demyelinated by Cuprizone

EGF-Coupled Gold Nanoparticles Increase the Expression of CNPase and the Myelin-Associated Proteins MAG, MOG, and MBP in the Septal Nucleus Demyelinated by Cuprizone

Myelin in Alzheimer’s disease: culprit or bystander?

Recent Insights into the Functional Role of AMPA Receptors in the Oligodendrocyte Lineage Cells In Vivo

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