Characterization of retinaldehyde dehydrogenase-2 induction in NG2-positive glia after spinal cord contusion injury

Johanna Kern, Kirsten Schrage, Guido C Koopmans, Elbert A Joosten, Peter McCaffery, Jörg Mey

Research output: Contribution to journalArticlepeer-review

24 Citations (Scopus)


The transcriptional activator retinoic acid (RA) supports axonal regeneration of several neuronal cell populations in vitro, and it has been suggested that its receptor RARbeta2 may be used to support axonal regeneration in the adult mammalian spinal cord. We have previously shown that spinal cord injury induces activity of the RA synthesizing enzyme retinaldehyde dehydrogenase (RALDH)2 in NG2-positive cells. This report quantifies the increase of RALDH2 protein in the injured spinal cord and characterizes the RALDH2/NG2 expressing cells probably as a unique RA synthesizing subpopulation of activated oligodendrocyte precursors or "polydendrocytes". In the uninjured spinal cord low levels of RALDH2 are present in oligodendrocytes as well as in the meninges and in blood vessels. Following injury there is a significant increase in RALDH2 in these latter two tissues and, given that the RALDH2/NG2 positive cells are clustered in the same area, this implies that these are specific foci of RA synthesis. It is presumed that these cells release RA in a paracrine fashion in the region of the wound; however, the RALDH2/NG2-immunoreactive cells expressed the retinoid receptors RARalpha, RARbeta, RXRalpha and RXRbeta, suggesting that RA also serves an autocrine function.
Original languageEnglish
Pages (from-to)7-16
Number of pages10
JournalInternational Journal of Developmental Neuroscience
Issue number1
Early online date18 Jan 2007
Publication statusPublished - Feb 2007


  • Aldehyde Oxidoreductases
  • Animals
  • Antigens
  • Enzyme Induction
  • Gene Expression Regulation
  • Immunohistochemistry
  • Male
  • Models, Biological
  • Neuroglia
  • Proteoglycans
  • Rats
  • Rats, Inbred Lew
  • Receptors, Retinoic Acid
  • Spinal Cord Injuries
  • Time Factors


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