Toward a transgenic mouse model of remyelination

S. Ferraresi, I. Lorenzetti, R. Nemni, J. Kamholz, M. L. Feltri, L. Wrabetz

Research output: Contribution to journalArticlepeer-review


The molecular mechanisms necessary for remyelination by oligodendrocytes remain unexplored. We previously characterized a myelin basic protein promoter-lacZ (MBP-lacZ) transgene whose expression is regulated uniquely during development, and also in pathological situations, suggesting that it may be a useful reporter of molecular mechanisms during remyelination. As a first step toward creating a transgenic mouse model of remyelination, we cultured oligodendrocytes from these transgenic mice and showed that expression of MBP-lacZ appeared in parallel with a marker of oligodendrocyte maturation, galactocerebroside (GC). In addition, basic fibroblast growth factor blocked the expression of both MBP-lacZ and GC in these cells. Therefore, expression of MBP-lacZ reflects not only the developmental stage of oligodendrocytes, but also extrinsic influences on oligodendrocytes. These data suggest that MBP-lacZ may be a useful marker in transgenic mouse models of remyelination.

Original languageEnglish
Pages (from-to)80-83
Number of pages4
JournalMultiple Sclerosis Journal
Issue number2
Publication statusPublished - Apr 1997


  • β-galactosidase
  • Fibroblast growth factor
  • Myelin basic protein promoter
  • Oligodendrocytes
  • Platelet derived growth factor
  • Remyelination

ASJC Scopus subject areas

  • Clinical Neurology


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