Oligodendrocyte progenitor migration in response to injury of glial monolayers requires the polysialic neural cell-adhesion molecule

M. J. Barral-Moran, V. Calaora, L. Vutskits, C. Wang, H. Zhang, P. Durbec, G. Rougon, J. Z. Kiss

Research output: Contribution to journalArticle

25 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)679-690
Number of pages12
JournalJournal of Neuroscience Research
Volume72
Issue number6
DOIs
Publication statusPublished - Jun 15 2003

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Keywords

  • Astrocyte
  • Cell adhesion molecules
  • Cell migration
  • Glial repair
  • O-2A progenitor

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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