Axoskeletal proteins prevent oligodendrocyte from toxic injury by upregulating survival, proliferation, and differentiation in vitro

TitreAxoskeletal proteins prevent oligodendrocyte from toxic injury by upregulating survival, proliferation, and differentiation in vitro
Type de publicationArticle de revue
AuteurFressinaud, Catherine , Eyer, Joël
EditeurElsevier
TypeArticle scientifique dans une revue à comité de lecture
Année2013
LangueAnglais
Date2013/02
Numéro3
Pagination306 - 313
Volume62
Titre de la revueNeurochemistry International
ISSN0197-0186
Mots-clésdifferentiation, Lysolecithin, neurofilament, Proliferation, Remyelination, Tubulin
Résumé en anglais

Neurofilaments (NF) are detected in the cerebrospinal fluid of multiple sclerosis (MS) patients, and their concentration correlates with disease severity. We recently demonstrated that NF and co-isolated proteins increase the proliferation and differentiation of oligodendrocytes (OL) in vitro. If these proteins are released in the extracellular environment in MS, they might then regulate remyelination by OL. To test this hypothesis we took advantage of a paradigm of OL toxic injury using lysophosphatidyl choline (LPC), which decreases proliferation and differentiation of surviving cells, and destroys myelin-like membranes. In OL cultures that have been treated with LPC, NF fractions as well as tubulin (TUB) significantly improved recovery: the number of OL progenitors (OLP, A2B5+ cells) increased by 100% and their proliferation by 200%, whereas differentiated (CNP+) and mature (MBP+) cells increased by 150% compared to cultures treated with LPC alone. When added at the time of LPC treatment, NF and TUB protected OL from LPC toxicity; they increased OLP by 90%, as well as the number of CNP+ and MBP+ OL by 65–110%, respectively, compared to cultures treated only with LPC. These effects were specific since irrelevant proteins (actin, skin proteins) were ineffective. This demonstrates that NF and TUB protect OL and increase OLP proliferation, as well as their survival, when challenged with LPC, without delaying differentiation and maturation in vitro. Thus, NF and TUB delivered following axonal damage in MS could participate in the regulation of remyelination through this process.

URL de la noticehttp://okina.univ-angers.fr/publications/ua9033
DOI10.1016/j.neuint.2012.12.012
Lien vers le document

http://dx.doi.org/10.1016/j.neuint.2012.12.012