Regulation and dysregulation of axon infrastructure by myelinating glia

Pan, Simon; Chan, Jonah R.

doi:10.1083/jcb.201702150

Cited by 42 publications

(33 citation statements)

References 178 publications

(273 reference statements)

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“…During myelination, molecular clustering occurs at the nodes of Ranvier which involves axonal adhesion molecule neurofascin 186, βIV spectrin, βII spectrin, ankyrin G, voltage-gated sodium channels, voltage-gated potassium channels, TAG-1 and actin, together with glial cell adhesion molecule neurofascin 155, axonal contactin and Caspr (Pan and Chan, 2017). Ankyrin deficiency alters the structure of the nodes of Ranvier and results in axonal degeneration (Saifetiarova et al, 2017).…”

Section: Development Of Oligodendroglia and Myelinmentioning

confidence: 99%

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

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Oligodendrocytes are in contact with neurons, wrap axons with a myelin sheath that protects their structural integrity, and facilitate nerve conduction. Oligodendrocytes also form a syncytium with astrocytes which interacts with neurons, promoting reciprocal survival mediated by activity and by molecules involved in energy metabolism and trophism. Therefore, oligodendrocytes are key elements in the normal functioning of the central nervous system. Oligodendrocytes are affected following different insults to the central nervous system including ischemia, traumatism, and inflammation. The term oligodendrogliopathy highlights the prominent role of altered oligodendrocytes in the pathogenesis of certain neurological diseases, not only in demyelinating diseases and most leukodystrophies, but also in aging and age-related neurodegenerative diseases with abnormal protein aggregates. Most of these diseases are characterized by the presence of abnormal protein deposits, forming characteristic and specific inclusions in neurons and astrocytes but also in oligodendrocytes, thus signaling their involvement in the disease. Emerging evidence suggests that such deposits in oligodendrocytes are not mere bystanders but rather are associated with functional alterations. Moreover, operative modifications in oligodendrocytes are also detected in the absence of oligodendroglial inclusions in certain diseases. The present review focuses first on general aspects of oligodendrocytes and precursors, and their development and functions, and then introduces and updates alterations and dysfunction of oligodendrocytes in selected neurodegenerative diseases with abnormal protein aggregates such as multiple system atrophy, Lewy body diseases, tauopathies, Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal lobar degeneration with TDP-43 inclusions (TDP-43 proteinopathies), and Creutzfeldt-Jakob´s disease as a prototypical human prionopathy.

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Section: Development Of Oligodendroglia and Myelinmentioning

confidence: 99%

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

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“…In keeping with this view, GS is frequently used as an astrocyte-specific marker (Armbruster et al, 2016; Habbas et al, 2015; Okuda et al, 2014; Papageorgiou et al, 2018; Theofilas et al, 2017; Tong et al, 2014). However, GS expression has also been reported in oligodendrocytes (Bernstein et al, 2014; Takasaki et al, 2010), glial cells known for producing myelin and ensheathing axons in the CNS (Pan and Chan, 2017). Although these results remain controversial (Anlauf and Derouiche, 2013; Jayakumar and Norenberg, 2016; Sun et al, 2017), it is of great physiological and clinical importance to identify all potential cellular and molecular components involved in the life cycle of glutamate.…”

Section: Introductionmentioning

confidence: 99%

Oligodendrocytes Support Neuronal Glutamatergic Transmission via Expression of Glutamine Synthetase

et al. 2019

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SUMMARY Glutamate has been implicated in a wide range of brain pathologies and is thought to be metabolized via the astrocyte-specific enzyme glutamine synthetase (GS). We show here that oligodendrocytes, the myelinating glia of the central nervous system, also express high levels of GS in caudal regions like the midbrain and the spinal cord. Selective removal of oligodendrocyte GS in mice led to reduced brain glutamate and glutamine levels and impaired glutamatergic synaptic transmission without disrupting myelination. Furthermore, animals lacking oligodendrocyte GS displayed deficits in cocaine-induced locomotor sensitization, a behavior that is dependent on glutamatergic signaling in the midbrain. Thus, oligodendrocytes support glutamatergic transmission through the actions of GS and may represent a therapeutic target for pathological conditions related to brain glutamate dysregulation.

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“…Glial cells are important for axonal function and synaptic plasticity, acting as integral mediators of neuronal connectivity (Stogsdill & Eroglu, 2017). In the central nervous system (CNS), oligodendrocyte progenitor cells (OPCs) mature into oligodendroglia, which associate with and ensheathe axons with myelin during development and after demyelination (Pan & Chan, 2017), thereby organizing the nodal, paranodal, and juxtaparanodal regions important for neuronal communication (Mitew et al, 2014). According to the newly proposed model of myelination, an oligodendrocyte process first contacts and ensheathes the axon, and then, proceeds wrapping the axon by extending the inner tongue of the process under the outer layer to generate multilayered compact myelin (Bercury & Macklin, 2015).…”

Section: Introductionmentioning

confidence: 99%

Ermin is a p116^RIP‐interacting protein promoting oligodendroglial differentiation and myelin maintenance

Wang

Liu

et al. 2020

Glia

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Myelin sheaths, which insulate the axons and ensure saltatory conduction of the nerve impulse, are generated and maintained via largely uncharacterized mechanisms. Ermin is an oligodendrocyte‐specific protein associated with the cytoskeleton, but how it regulates cytoskeletal remodeling during oligodendrocyte differentiation and its role in myelin maintenance are not clear. To address this, we generated mice constitutively deficient for Ermn, the Ermin‐coding gene. We found that aged Ermn‐knockout mice exhibit an aberrant myelin architecture, with splitting of myelin layers, peeling of the myelin sheath from axons, and breakdown of myelinated fibers. As a result, these mice had remarkably impaired motor coordination. Ermn knockout also accelerated cuprizone‐induced demyelination and exacerbated the associated movement disorders. Ermin was found to contribute to oligodendrocyte morphogenesis by associating with the myosin phosphatase Rho interacting protein (Mprip/p116RIP) and inactivating RhoA, a GTPase that controls cytoskeletal rearrangement in differentiating cells. These findings provide novel insights into the mechanisms regulating oligodendroglial differentiation, the maintenance of the myelin sheaths, and remyelination.

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Regulation and dysregulation of axon infrastructure by myelinating glia

Abstract: Pan and Chan discuss the role of myelinating glia in axonal development and the impact of demyelination on axon degeneration.

Cited by 42 publications

References 178 publications

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Oligodendrocytes Support Neuronal Glutamatergic Transmission via Expression of Glutamine Synthetase

Ermin is a p116^RIP‐interacting protein promoting oligodendroglial differentiation and myelin maintenance

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Regulation and dysregulation of axon infrastructure by myelinating glia

Abstract: Pan and Chan discuss the role of myelinating glia in axonal development and the impact of demyelination on axon degeneration.

Cited by 42 publications

References 178 publications

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Oligodendrocytes Support Neuronal Glutamatergic Transmission via Expression of Glutamine Synthetase

Ermin is a p116RIP‐interacting protein promoting oligodendroglial differentiation and myelin maintenance

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Ermin is a p116^RIP‐interacting protein promoting oligodendroglial differentiation and myelin maintenance