A Glance at the Molecules That Regulate Oligodendrocyte Myelination

Wang, Shunqi; Wang, Yingxing; Zou, Suqi

doi:10.3390/cimb44050149

Cited by 13 publications

(16 citation statements)

References 204 publications

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“…While the previous transcriptomic studies (Chitu et al, 2020) showed that Csf1r +/À microglia were dyshomeostatic, they did not produce evidence of classical neuroinflammation or identify candidate mediators of microglia toxicity to oligodendrocytes and neurons. In contrast, in the present work, proteomic profiling of isolated microglia raises the possibility that altered eicosanoid production (Figure 4c,f) might contribute to the functional alteration of both microglia (Fadok et al, 1998;Michael et al, 2019) and oligodendrocytes (Wang, Wang, & Zou, 2022), an aspect that deserves further investigation. In addition, Csf1r heterozygosity leads to decreased levels of parathymosin in microglia.…”

Section: Discussioncontrasting

confidence: 70%

Prophylactic effect of chronic immunosuppression in a mouse model of CSF‐1 receptor‐related leukoencephalopathy

Chitu,

Biundo,

Oppong‐Asare

et al. 2023

Glia

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Mutations leading to colony‐stimulating factor‐1 receptor (CSF‐1R) loss‐of‐function or haploinsufficiency cause CSF1R‐related leukoencephalopathy (CRL), an adult‐onset disease characterized by loss of myelin and neurodegeneration, for which there is no effective therapy. Symptom onset usually occurs in the fourth decade of life and the penetrance of disease in carriers is high. However, familial studies have identified a few carriers of pathogenic CSF1R mutations that remain asymptomatic even in their seventh decade of life, raising the possibility that the development and severity of disease might be influenced by environmental factors. Here we report new cases in which long‐term glucocorticoid treatment is associated with asymptomatic status in elder carriers of pathogenic CSF‐1R mutations. The main objective of the present study was to investigate the link between chronic immunosuppression initiated pre‐symptomatically and resistance to the development of symptomatic CRL, in the Csf1r+/− mouse model. We show that chronic prednisone administration prevents the development of memory, motor coordination and social interaction deficits, as well as the demyelination, neurodegeneration and microgliosis associated with these deficits. These findings are in agreement with the preliminary clinical observations and support the concept that pre‐symptomatic immunosuppression is protective in patients carrying pathogenic CSF1R variants associated with CRL. Proteomic analysis of microglia and oligodendrocytes indicates that prednisone suppresses processes involved in microglial activation and alleviates senescence and improves fitness of oligodendrocytes. This analysis also identifies new potential targets for therapeutic intervention.

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Section: Discussioncontrasting

confidence: 70%

Prophylactic effect of chronic immunosuppression in a mouse model of CSF‐1 receptor‐related leukoencephalopathy

Chitu,

Biundo,

Oppong‐Asare

et al. 2023

Glia

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“…It is widely described that AKT signaling is required for proper myelination and it is dysregulated in white matter abnormalities ( Wang et al, 2022 ). It has also been described that AKT1/2/3 Knock-out mice lack mature OLs ( Wang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…It has also been described that AKT1/2/3 Knock-out mice lack mature OLs ( Wang et al, 2021 ). Different molecules have been indicated as both AKT activators (e.g., neuregulin1, ErbB, and ECM proteins) and downstream regulators (e.g., mTOR1, mTOR2, TSC1/2, RHEB, and Sox10 through FoxO1) ( Wood et al, 2013 ; Wang et al, 2022 ). In the present study we provide solid evidence that also NGF/TRKA pathway activates AKT during OPC differentiation/maturation.…”

Section: Discussionmentioning

confidence: 99%

Nerve growth factor promotes differentiation and protects the oligodendrocyte precursor cells from in vitro hypoxia/ischemia

Baldassarro

Cescatti²,

Rocco³

et al. 2023

Front. Neurosci.

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IntroductionNerve growth factor (NGF) is a pleiotropic molecule acting on different cell types in physiological and pathological conditions. However, the effect of NGF on the survival, differentiation and maturation of oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), the cells responsible for myelin formation, turnover, and repair in the central nervous system (CNS), is still poorly understood and heavily debated.MethodsHere we used mixed neural stem cell (NSC)-derived OPC/astrocyte cultures to clarify the role of NGF throughout the entire process of OL differentiation and investigate its putative role in OPC protection under pathological conditions.ResultsWe first showed that the gene expression of all the neurotrophin receptors (TrkA, TrkB, TrkC, and p75NTR) dynamically changes during the differentiation. However, only TrkA and p75NTR expression depends on T3-differentiation induction, as Ngf gene expression induction and protein secretion in the culture medium. Moreover, in the mixed culture, astrocytes are the main producer of NGF protein, and OPCs express both TrkA and p75NTR. NGF treatment increases the percentage of mature OLs, while NGF blocking by neutralizing antibody and TRKA antagonist impairs OPC differentiation. Moreover, both NGF exposure and astrocyte-conditioned medium protect OPCs exposed to oxygenglucose deprivation (OGD) from cell death and NGF induces an increase of AKT/pAKT levels in OPCs nuclei by TRKA activation.DiscussionThis study demonstrated that NGF is implicated in OPC differentiation, maturation, and protection in the presence of metabolic challenges, also suggesting implications for the treatment of demyelinating lesions and diseases.

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“…Recent research has demonstrated that TNF-α from pro-regenerative macrophages can activate ERG progenitors and promote neurogenesis by non-developmental signals through the expression of HDAC1 [ 11 ]. Moreover, HDAC1 is crucial for oligodendrocyte regeneration, proliferation, and nerve remyelination [ 64 , 65 ]. Taken together, these findings suggest that macrophage-secreted TNF-α can regulate ERG motor neuron progenitors and oligodendrocyte differentiation, ultimately promoting regenerative neurogenesis.…”

Section: Macrophage Tnf-α Signaling May Regulate Pmn Progenitor Cell ...mentioning

confidence: 99%

Macrophage–Neuroglia Interactions in Promoting Neuronal Regeneration in Zebrafish

Zeng

2023

IJMS

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The human nervous system exhibits limited regenerative capabilities following damage to the central nervous system (CNS), leading to a scarcity of effective treatments for nerve function recovery. In contrast, zebrafish demonstrate remarkable regenerative abilities, making them an ideal model for studying the modulation of inflammatory processes after injury. Such research holds significant translational potential to enhance our understanding of recovery from damage and disease. Macrophages play a crucial role in tissue repair and regeneration, with their subpopulations indirectly promoting axonal regeneration through developmental signals. The AP-1 signaling pathway, mediated by TNF/Tnfrsf1a, can elevate HDAC1 expression and facilitate regeneration. Furthermore, following spinal cord injury (SCI), pMN progenitors have been observed to switch between oligodendrocyte and motor neuron fates, with macrophage-secreted TNF-α potentially regulating the differentiation of ependymal–radial glia progenitors and oligodendrocytes. Radial glial cells (RGs) are also essential for CNS regeneration in zebrafish, as they perform neurogenesis and gliogenesis, with specific RG subpopulations potentially existing for the generation of neurons and oligodendrocytes. This review article underscores the critical role of macrophages and their subpopulations in tissue repair and regeneration, focusing on their secretion of TNF-α, which promotes axonal regeneration in zebrafish. We also offer insights into the molecular mechanisms underlying TNF-α’s ability to facilitate axonal regeneration and explore the potential of pMN progenitor cells and RGs following SCI in zebrafish. The review concludes with a discussion of various unresolved questions in the field, and ideas are suggested for future research. Studying innate immune cell interactions with neuroglia following injury may lead to the development of novel strategies for treating the inflammatory processes associated with regenerative medicine, which are commonly observed in injury and disease.

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A Glance at the Molecules That Regulate Oligodendrocyte Myelination

Cited by 13 publications

References 204 publications

Prophylactic effect of chronic immunosuppression in a mouse model of CSF‐1 receptor‐related leukoencephalopathy

Prophylactic effect of chronic immunosuppression in a mouse model of CSF‐1 receptor‐related leukoencephalopathy

Nerve growth factor promotes differentiation and protects the oligodendrocyte precursor cells from in vitro hypoxia/ischemia

Macrophage–Neuroglia Interactions in Promoting Neuronal Regeneration in Zebrafish

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