UZH-Logo

Maintenance Infos

NG2 expressed by macrophages and oligodendrocyte precursor cells is dispensable in experimental autoimmune encephalomyelitis


Moransard, M; Dann, A; Staszewski, O; Fontana, A; Prinz, M; Suter, T (2011). NG2 expressed by macrophages and oligodendrocyte precursor cells is dispensable in experimental autoimmune encephalomyelitis. Brain: A Journal of Neurology, 134(Pt. 5):1315-1330.

Abstract

Increased expression of the chondroitin proteoglycan NG2 is a prominent feature in central nervous system injury with unknown cellular source and biological relevance. Here, we describe the first detailed analysis of experimental autoimmune encephalomyelitis in NG2 knockout mice and NG2 knockout bone marrow chimeras. We show that both macrophages and oligodendrocyte progenitor cells express and secrete NG2 in response to transforming growth factor-β. A subpopulation of macrophages expresses NG2 within leucocyte infiltrates in the central nervous system, but only oligodendrocyte progenitor cells contribute to NG2 accumulation. Notably, NG2 plays no role in experimental autoimmune encephalomyelitis initiation, progression or recuperation. In concurrence, the immune response is unaltered in NG2-deficient mice as are the extent of central nervous system damage and degree of remyelination.

Abstract

Increased expression of the chondroitin proteoglycan NG2 is a prominent feature in central nervous system injury with unknown cellular source and biological relevance. Here, we describe the first detailed analysis of experimental autoimmune encephalomyelitis in NG2 knockout mice and NG2 knockout bone marrow chimeras. We show that both macrophages and oligodendrocyte progenitor cells express and secrete NG2 in response to transforming growth factor-β. A subpopulation of macrophages expresses NG2 within leucocyte infiltrates in the central nervous system, but only oligodendrocyte progenitor cells contribute to NG2 accumulation. Notably, NG2 plays no role in experimental autoimmune encephalomyelitis initiation, progression or recuperation. In concurrence, the immune response is unaltered in NG2-deficient mice as are the extent of central nervous system damage and degree of remyelination.

Citations

17 citations in Web of Science®
15 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

255 downloads since deposited on 04 Mar 2012
23 downloads since 12 months
Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Immunology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2011
Deposited On:04 Mar 2012 10:08
Last Modified:05 Apr 2016 15:34
Publisher:Oxford University Press
ISSN:0006-8950
Publisher DOI:https://doi.org/10.1093/brain/awr070
PubMed ID:21596769

Download

[img]
Preview
Content: Accepted Version
Filetype: PDF
Size: 746kB
View at publisher

TrendTerms

TrendTerms displays relevant terms of the abstract of this publication and related documents on a map. The terms and their relations were extracted from ZORA using word statistics. Their timelines are taken from ZORA as well. The bubble size of a term is proportional to the number of documents where the term occurs. Red, orange, yellow and green colors are used for terms that occur in the current document; red indicates high interlinkedness of a term with other terms, orange, yellow and green decreasing interlinkedness. Blue is used for terms that have a relation with the terms in this document, but occur in other documents.
You can navigate and zoom the map. Mouse-hovering a term displays its timeline, clicking it yields the associated documents.

Author Collaborations