Oligodendrocyte progenitor migration in response to injury of glial monolayers requires the polysialic neural cell-adhesion molecule
✍ Scribed by M.-J. Barral-Moran; V. Calaora; L. Vutskits; C. Wang; H. Zhang; P. Durbec; G. Rougon; J.Z. Kiss
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 669 KB
- Volume
- 72
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
Injury to the nervous system results in reactive astrogliosis that is a critical determinant of neuronal regeneration. To analyze glial responses to mechanical injury and the role of the polysialic neural cell adhesion molecule (PSA‐NCAM) in this process, we established primary glia cultures from newborn rat cerebral cortex. Scratching a confluent monolayer of primary glial cells resulted in two major events: rapid migration of oligodendrocyte progenitor‐like (O‐2A) cells into the wounded area and development of polarized morphology of type 1 astrocytes at the wound edge. Migrating O‐2A progenitors had a bipolar morphology and exhibited A2B5 and O4 immunolabeling. Once these cells were established inside the wounded area, they lost A2B5 immunoreactivity and differentiated into glial fibrillary acidic protein‐positive astrocytes. Migrating O‐2A cells expressed PSA‐NCAM, but type 1 astrocytes at the wound edge did not. Treatment of wounded cultures with Endo‐N, which specifically removes PSA from the surface of cells, resulted in a significant decrease in O‐2A cell migration into the wounded area and completely blocked the wound closure. Video time‐lapse analysis showed that, in the presence of Endo‐N, O‐2A cells remained motile and migrated short distances but did not move away from the monolayer. These results demonstrate that O‐2A progenitors contribute to reactive astrogliosis in culture and that PSA‐NCAM is involved in this process by regulating cell migration. © 2003 Wiley‐Liss, Inc.