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Oligodendrocyte Progenitor Cells Proliferate And Survive In An Immature State Following Treatment With An Axolemma-Enriched Fraction.

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Title: Oligodendrocyte Progenitor Cells Proliferate And Survive In An Immature State Following Treatment With An Axolemma-Enriched Fraction.
Alternative Title: Short running title: Effect of AEF on OPC
Author(s): Becker-Catania, Sara G.; Nelson, Julie K.; Olivares, Shantel; Chen, Shu-Jen; DeVries, George H.
Abstract: The ability of an axolemma-enriched fraction (AEF) to influence the proliferation, survival, and differentiation of oligodendrocyte progenitor cells (OPC) was evaluated. Following addition of AEF to cultured OPC, the AEF associated with the outer surface of OPC so that subsequent metabolic events were likely mediated by direct AEF-OPC contact. Addition of AEF to the cultured OPC resulted in a dose- and time-dependent increase in proliferation which was partially dependent on Akt and MAP kinase activation. The major mitogen in a soluble 2.0 M NaCl extract of the AEF was identified as aFGF and accounted for 50% of the mitogenicity. The remaining 50% of the mitogenicity had properties consistent with bFGF but was not unequivocally identified. Under conditions that limit the survival of OPC in culture, AEF treatment prolonged the survival of the OPC. Antigenic and morphological examination of the AEF-treated OPC indicated that the AEF treatment helped the OPC survive in a more immature state. The potential downstream metabolic pathways potentially activated in OPC by AEF and the consequences of these activated pathways are discussed. The results of these studies are consistent with the view that direct contact of axons with OPC stimulates their proliferation and survival while preventing their differentiation.
Issue Date: 2011
Publisher: Portland Press
Citation Info: Becker-Catania, S. G., Nelson, J. K., Olivares, S., Chen, S. J., & DeVries, G. H. 2011. Oligodendrocyte progenitor cells proliferate and survive in an immature state following treatment with an axolemma-enriched fraction. Asn Neuro, 3(1): 51-67. DOI: 10.1042/AN20100035
Type: Article
Description: The final version of record is available at DOI: 10.1042/AN20100035
ISSN: 1759-0914
Sponsor: This research has been supported by grant from the National Institute of Neurological Disease and Stroke (NIH grant NS43419-01A), Salary support for G.H.D.V. was provided by a Research Career Service Award from the Department of Veteran Affairs.
Date Available in INDIGO: 2012-08-15

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