Publication

Identification of a microglia phenotype supportive of remyelination

Olah, M., Amor, S., Brouwer, N., Vinet, J., Eggen, B., Biber, K. & Boddeke, H. W. G. M., Feb-2012, In : Glia. 60, 2, p. 306-321 16 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Olah, M., Amor, S., Brouwer, N., Vinet, J., Eggen, B., Biber, K., & Boddeke, H. W. G. M. (2012). Identification of a microglia phenotype supportive of remyelination. Glia, 60(2), 306-321. https://doi.org/10.1002/glia.21266

Author

Olah, Marta ; Amor, Sandra ; Brouwer, Nieske ; Vinet, Jonathan ; Eggen, Bart ; Biber, Knut ; Boddeke, Hendrikus W. G. M. / Identification of a microglia phenotype supportive of remyelination. In: Glia. 2012 ; Vol. 60, No. 2. pp. 306-321.

Harvard

Olah, M, Amor, S, Brouwer, N, Vinet, J, Eggen, B, Biber, K & Boddeke, HWGM 2012, 'Identification of a microglia phenotype supportive of remyelination', Glia, vol. 60, no. 2, pp. 306-321. https://doi.org/10.1002/glia.21266

Standard

Identification of a microglia phenotype supportive of remyelination. / Olah, Marta; Amor, Sandra; Brouwer, Nieske; Vinet, Jonathan; Eggen, Bart; Biber, Knut; Boddeke, Hendrikus W. G. M.

In: Glia, Vol. 60, No. 2, 02.2012, p. 306-321.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Olah M, Amor S, Brouwer N, Vinet J, Eggen B, Biber K et al. Identification of a microglia phenotype supportive of remyelination. Glia. 2012 Feb;60(2):306-321. https://doi.org/10.1002/glia.21266


BibTeX

@article{ade057195dea4e989781c86f2167bb87,
title = "Identification of a microglia phenotype supportive of remyelination",
abstract = "In multiple sclerosis, endogenous oligodendrocyte precursor cells (OPCs) attempt to remyelinate areas of myelin damage. During disease progression, however, these attempts fail. It has been suggested that modulating the inflammatory environment of the lesion might provide a promising therapeutic approach to promote endogenous remyelination. Microglia are known to play a central role in neuroinflammatory processes. To investigate the microglia phenotype that supports remyelination, we performed genome-wide gene expression analysis of microglia from the corpus callosum during demyelination and remyelination in the mouse cuprizone model, in which remyelination spontaneously occurs after an episode of toxin-induced primary demyelination. We provide evidence for the existence of a microglia phenotype that supports remyelination already at the onset of demyelination and persists throughout the remyelination process. Our data show that microglia are involved in the phagocytosis of myelin debris and apoptotic cells during demyelination. Furthermore, they express a cytokine and chemokine repertoire enabling them to activate and recruit endogenous OPCs to the lesion site and deliver trophic support during remyelination. This study not only provides a detailed transcriptomic analysis of the remyelination-supportive microglia phenotype but also reinforces the notion that the primary function of microglia is the maintenance of tissue homeostasis and the support of regeneration already at the earliest stages in the development of demyelinating lesions. (c) 2011 Wiley Periodicals, Inc.",
keywords = "microglia phenotype, remyelination, preactive lesions, CUPRIZONE-INDUCED DEMYELINATION, CENTRAL-NERVOUS-SYSTEM, BLOOD-BRAIN-BARRIER, EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS, LEUKOCYTE PROTEASE INHIBITOR, MULTIPLE-SCLEROSIS, CNS DEMYELINATION, IMMUNE-RESPONSES, GENE-EXPRESSION, MACROPHAGE-DEPLETION",
author = "Marta Olah and Sandra Amor and Nieske Brouwer and Jonathan Vinet and Bart Eggen and Knut Biber and Boddeke, {Hendrikus W. G. M.}",
year = "2012",
month = "2",
doi = "10.1002/glia.21266",
language = "English",
volume = "60",
pages = "306--321",
journal = "Glia",
issn = "0894-1491",
publisher = "Wiley",
number = "2",

}

RIS

TY - JOUR

T1 - Identification of a microglia phenotype supportive of remyelination

AU - Olah, Marta

AU - Amor, Sandra

AU - Brouwer, Nieske

AU - Vinet, Jonathan

AU - Eggen, Bart

AU - Biber, Knut

AU - Boddeke, Hendrikus W. G. M.

PY - 2012/2

Y1 - 2012/2

N2 - In multiple sclerosis, endogenous oligodendrocyte precursor cells (OPCs) attempt to remyelinate areas of myelin damage. During disease progression, however, these attempts fail. It has been suggested that modulating the inflammatory environment of the lesion might provide a promising therapeutic approach to promote endogenous remyelination. Microglia are known to play a central role in neuroinflammatory processes. To investigate the microglia phenotype that supports remyelination, we performed genome-wide gene expression analysis of microglia from the corpus callosum during demyelination and remyelination in the mouse cuprizone model, in which remyelination spontaneously occurs after an episode of toxin-induced primary demyelination. We provide evidence for the existence of a microglia phenotype that supports remyelination already at the onset of demyelination and persists throughout the remyelination process. Our data show that microglia are involved in the phagocytosis of myelin debris and apoptotic cells during demyelination. Furthermore, they express a cytokine and chemokine repertoire enabling them to activate and recruit endogenous OPCs to the lesion site and deliver trophic support during remyelination. This study not only provides a detailed transcriptomic analysis of the remyelination-supportive microglia phenotype but also reinforces the notion that the primary function of microglia is the maintenance of tissue homeostasis and the support of regeneration already at the earliest stages in the development of demyelinating lesions. (c) 2011 Wiley Periodicals, Inc.

AB - In multiple sclerosis, endogenous oligodendrocyte precursor cells (OPCs) attempt to remyelinate areas of myelin damage. During disease progression, however, these attempts fail. It has been suggested that modulating the inflammatory environment of the lesion might provide a promising therapeutic approach to promote endogenous remyelination. Microglia are known to play a central role in neuroinflammatory processes. To investigate the microglia phenotype that supports remyelination, we performed genome-wide gene expression analysis of microglia from the corpus callosum during demyelination and remyelination in the mouse cuprizone model, in which remyelination spontaneously occurs after an episode of toxin-induced primary demyelination. We provide evidence for the existence of a microglia phenotype that supports remyelination already at the onset of demyelination and persists throughout the remyelination process. Our data show that microglia are involved in the phagocytosis of myelin debris and apoptotic cells during demyelination. Furthermore, they express a cytokine and chemokine repertoire enabling them to activate and recruit endogenous OPCs to the lesion site and deliver trophic support during remyelination. This study not only provides a detailed transcriptomic analysis of the remyelination-supportive microglia phenotype but also reinforces the notion that the primary function of microglia is the maintenance of tissue homeostasis and the support of regeneration already at the earliest stages in the development of demyelinating lesions. (c) 2011 Wiley Periodicals, Inc.

KW - microglia phenotype

KW - remyelination

KW - preactive lesions

KW - CUPRIZONE-INDUCED DEMYELINATION

KW - CENTRAL-NERVOUS-SYSTEM

KW - BLOOD-BRAIN-BARRIER

KW - EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS

KW - LEUKOCYTE PROTEASE INHIBITOR

KW - MULTIPLE-SCLEROSIS

KW - CNS DEMYELINATION

KW - IMMUNE-RESPONSES

KW - GENE-EXPRESSION

KW - MACROPHAGE-DEPLETION

U2 - 10.1002/glia.21266

DO - 10.1002/glia.21266

M3 - Article

VL - 60

SP - 306

EP - 321

JO - Glia

JF - Glia

SN - 0894-1491

IS - 2

ER -

ID: 5457482