Facial nerve lesion response; strain differences but no involvement of IFN-gamma, STAT4 or STAT6

Neuroreport. 2002 Sep 16;13(13):1589-93. doi: 10.1097/00001756-200209160-00003.

Abstract

Facial nerve lesions lead to a retrograde response characterized by activation of glia surrounding axotomized motoneurons and up-regulation of immunological cell surface molecules such as major histocompatibility complex (MHC) antigens. Cytokines, in particular interferon-gamma, are potent inducers of MHC expression and glial activation. We have here tested whether axotomy-induced activation is changed in transgenic mouse strains lacking components of the IFN-gamma signaling pathway, STAT4 or STAT6. No differences regarding astrocyte activation, ss2-microglobulin or MHC class I expression were discernible as compared to wild type controls. In contrast, there were conspicuous differences in the reaction between the examined wild type strains (C57BL/6J, BALB/c and 129/SvJ), suggesting considerable polymorphisms in the genetic regulation of these events, however, not involving IFN-gamma, STAT4 or STAT6.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axotomy
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / immunology*
  • Facial Nerve Injuries / genetics
  • Facial Nerve Injuries / immunology*
  • Female
  • GAP-43 Protein / genetics
  • Gene Expression Regulation / physiology
  • Glial Fibrillary Acidic Protein / genetics
  • Gliosis / genetics
  • Gliosis / immunology
  • Histocompatibility Antigens / genetics
  • Histocompatibility Antigens / immunology
  • Interferon Regulatory Factor-1
  • Interferon-gamma / genetics
  • Interferon-gamma / immunology*
  • Male
  • Mice
  • Mice, Inbred Strains / genetics
  • Mice, Inbred Strains / growth & development*
  • Mice, Knockout
  • Motor Neurons / immunology
  • Motor Neurons / metabolism
  • Motor Neurons / pathology
  • Neuroglia / immunology
  • Neuroglia / metabolism
  • Phosphoproteins / genetics
  • RNA, Messenger / metabolism
  • Retrograde Degeneration / genetics
  • Retrograde Degeneration / immunology*
  • STAT4 Transcription Factor
  • STAT6 Transcription Factor
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • Trans-Activators / genetics
  • Trans-Activators / immunology*
  • Up-Regulation / physiology
  • beta 2-Microglobulin / genetics

Substances

  • DNA-Binding Proteins
  • GAP-43 Protein
  • Glial Fibrillary Acidic Protein
  • Histocompatibility Antigens
  • Interferon Regulatory Factor-1
  • Irf1 protein, mouse
  • Phosphoproteins
  • RNA, Messenger
  • STAT4 Transcription Factor
  • STAT6 Transcription Factor
  • Stat4 protein, mouse
  • Stat6 protein, mouse
  • Trans-Activators
  • beta 2-Microglobulin
  • Interferon-gamma