Galectin-4, a Negative Regulator of Oligodendrocyte Differentiation, Is Persistently Present in Axons and Microglia/Macrophages in Multiple Sclerosis Lesions

Jong, Charlotte G H M de; Stancic, Mirjana; Pinxterhuis, Tineke H.; Horssen, Jack van; Dam, Anne‐Marie van; Gabius, Hans‐Joachim; Baron, Wia

doi:10.1093/jnen/nly081

Cited by 16 publications

(19 citation statements)

References 87 publications

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“…2). In vitro analysis revealed that galectin-4 is not secreted by microglia and macrophages [179]. In addition, galectin-4 protein expression is upregulated in cultured alternatively activated microglia and macrophages and present in both the cytoplasm and nucleus, suggesting that it may add to their pro-regenerative properties.…”

Section: Interplay Of Astrocytes and Phagocytosing Cells Via Galectinsmentioning

confidence: 95%

“…2.3b). Remarkably, and in contrast to developmental myelination, galectin-4 resides also in the nucleus of microglia/macrophages upon cuprizone-induced myelination ( [179], Fig. 2).…”

Section: Interplay Of Astrocytes and Phagocytosing Cells Via Galectinsmentioning

confidence: 99%

“…Galectin-1 is prominently expressed in neurons and upregulated during sensory and motor neuron development [117,118]. Its presence guides primary olfactory and somatosensory axons and promotes neurite sprouting, both in vitro and in vivo, i.e., as shown by aberrant [151,221] Cuprizone-induced demyelination (Lgals3 −/− 129Sv mice) Increased emigration of SVZ cells to demyelinated areas and no effect on OPC differentiation Controls local inflammation in the SVZ and limits SVZ progenitor emigration [220] gal-4 Cuprizone-induced demyelination (C57Bl/6 mice) Re-expressed in axons and present in microglia/macrophages Neuronal re-expression and secretion of gal-4 may inhibit OPC differentiation [124,179] In vitro gal-1 Astrocytes (primary cell culture F344/N Slc rats, treatment)…”

Section: Galectins In Neuronal Functionmentioning

confidence: 99%

“…Therefore, remyelination morphologically resembles developmental myelination. In fact, some axonal factors including NCAM with its polysialic acid chains (PSA-NCAM), galectin-4 and LINGO-1 that are involved in the regulation of developmental myelination are re-expressed upon injury [20,22,[177][178][179]. An additional level of regulatory factors, mainly provided by microglia and astrocytes, is required to limit inflammation and demyelination and to clear myelin debris.…”

Section: Regulation Of Remyelination: a Major Role Of Microglia And Amentioning

confidence: 99%

“…2). Galectin-4 is transiently re-expressed on axons upon cuprizone-induced demyelination ( [179], Fig. 2.3).…”

Section: Interplay Of Astrocytes and Phagocytosing Cells Via Galectinsmentioning

confidence: 99%

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The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

Jong

Gabius

Baron

2019

Cell. Mol. Life Sci.

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Multiple sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system with unknown etiology. Currently approved disease-modifying treatment modalities are immunomodulatory or immunosuppressive. While the applied drugs reduce the frequency and severity of the attacks, their efficacy to regenerate myelin membranes and to halt disease progression is limited. To achieve such therapeutic aims, understanding biological mechanisms of remyelination and identifying factors that interfere with remyelination in MS can give respective directions. Such a perspective is given by the emerging functional profile of galectins. They form a family of tissue lectins, which are potent effectors in processes as diverse as adhesion, apoptosis, immune mediator release or migration. This review focuses on endogenous and exogenous roles of galectins in glial cells such as oligodendrocytes, astrocytes and microglia in the context of de-and (re)myelination and its dysregulation in MS. Evidence is arising for a cooperation among family members so that timed expression and/or secretion of galectins-1, -3 and -4 result in modifying developmental myelination, (neuro)inflammatory processes, de-and remyelination. Dissecting the mechanisms that underlie the distinct activities of galectins and identifying galectins as target or tool to modulate remyelination have the potential to contribute to the development of novel therapeutic strategies for MS.Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Section: Interplay Of Astrocytes and Phagocytosing Cells Via Galectinsmentioning

confidence: 95%

“…2.3b). Remarkably, and in contrast to developmental myelination, galectin-4 resides also in the nucleus of microglia/macrophages upon cuprizone-induced myelination ( [179], Fig. 2).…”

Section: Interplay Of Astrocytes and Phagocytosing Cells Via Galectinsmentioning

confidence: 99%

Section: Galectins In Neuronal Functionmentioning

confidence: 99%

Section: Regulation Of Remyelination: a Major Role Of Microglia And Amentioning

confidence: 99%

“…2). Galectin-4 is transiently re-expressed on axons upon cuprizone-induced demyelination ( [179], Fig. 2.3).…”

Section: Interplay Of Astrocytes and Phagocytosing Cells Via Galectinsmentioning

confidence: 99%

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The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

Jong

Gabius

Baron

2019

Cell. Mol. Life Sci.

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Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system

Mangale

Syage

Ekiz

et al. 2020

Glia

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The present study examines functional contributions of microglia in host defense, demyelination, and remyelination following infection of susceptible mice with a neurotropic coronavirus. Treatment with PLX5622, an inhibitor of colony stimulating factor 1 receptor (CSF1R) that efficiently depletes microglia, prior to infection of the central nervous system (CNS) with the neurotropic JHM strain of mouse hepatitis virus (JHMV) resulted in increased mortality compared with control mice that correlated with impaired control of viral replication. Single cell RNA sequencing (scRNASeq) of CD45+ cells isolated from the CNS revealed that PLX5622 treatment resulted in muted CD4+ T cell activation profile that was associated with decreased expression of transcripts encoding MHC class II and CD86 in macrophages but not dendritic cells. Evaluation of spinal cord demyelination revealed a marked increase in white matter damage in PLX5622‐treated mice that corresponded with elevated expression of transcripts encoding disease‐associated proteins Osteopontin (Spp1), Apolipoprotein E (Apoe), and Triggering receptor expressed on myeloid cells 2 (Trem2) that were enriched within macrophages. In addition, PLX5622 treatment dampened expression of Cystatin F (Cst7), Insulin growth factor 1 (Igf1), and lipoprotein lipase (Lpl) within macrophage populations which have been implicated in promoting repair of damaged nerve tissue and this was associated with impaired remyelination. Collectively, these findings argue that microglia tailor the CNS microenvironment to enhance control of coronavirus replication as well as dampen the severity of demyelination and influence repair.

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Probing sulfatide-tissue lectin recognition with functionalized glycodendrimersomes

et al. 2021

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Galectin-4, a Negative Regulator of Oligodendrocyte Differentiation, Is Persistently Present in Axons and Microglia/Macrophages in Multiple Sclerosis Lesions

Cited by 16 publications

References 87 publications

The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis

Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system

Probing sulfatide-tissue lectin recognition with functionalized glycodendrimersomes

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