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Oligodendrocyte‐type 2 Astrocyte Progenitors Use a Metalloendoprotease to Spread and Migrate on CNS Myelin
Author(s) -
Amberger Verena R.,
AvellanaAdalid Virginia,
Hensel Tamara,
Evercooren Anne BaronVan,
Schwab Martin E.
Publication year - 1997
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1997.tb01363.x
Subject(s) - oligodendrocyte , myelin , neurite , astrocyte , progenitor cell , microbiology and biotechnology , biology , neuroglia , central nervous system , neuroscience , immunology , in vitro , stem cell , biochemistry
Oligodendrocyte‐type 2 astrocyte (O‐2A) progenitors are highly motile cells which migrate in the developing and adult central nervous system (CNS). Adult CNS myelin, however, contains inhibitory proteins, the neurite growth inhibitors NI 35/250, which block neurite outgrowth and spreading of many different cell types, such as astrocytes and fibroblasts. In the present study we investigated the spreading of dissociated cells and migration out of aggregates (‘spheres’) of primary O‐2A cultures and of a glial precursor cell line (CG‐4) on purified CNS myelin and on CNS tissue. Primary O‐2A progenitors and CG‐4 cells quickly attached to and spread on CNS myelin‐coated culture dishes, showing no inhibition by the neurite growth inhibitors. CG‐4 cells migrated with a velocity of 30 pm/h on a CNS myelin protein extract and at 5.7 μm/h on adult spinal cord tissue. Both cell spreading and migration on a CNS substrate could be specifically blocked by metalloprotease blockers like o‐phenanthroline and the tetrapeptide carbobenzoxy‐phe‐ala‐phe‐tyr‐amide, whereas blockers of the serine, aspartyl and cysteine proteases had no effect. On differentiation to astrocytes, the O‐2A progenitors lost their ability to spread on CNS myelin. These results suggest the crucial involvement of a metalloprotease in the mechanism of migration on a CNS substrate. In vivo , migration of oligodendrocyte progenitors may be an important aspect of myelin repair following local traumatic, inflammatory or toxin‐induced myelin loss.