Huntingtin inclusions do not down-regulate specific genes in the R6/2 Huntington's disease mouse

Eur J Neurosci. 2006 Jun;23(12):3171-5. doi: 10.1111/j.1460-9568.2006.04871.x.

Abstract

Transcriptional dysregulation is a central pathogenic mechanism in Huntington's disease (HD); HD and transgenic mouse models of HD demonstrate down-regulation of specific genes at the level of mRNA expression. Furthermore, neuronal intranuclear inclusions (NIIs) have been identified in the brains of R6/2 mice and HD patients. One possibility is that NIIs contribute to transcriptional dysregulation by sequestering transcription factors. We therefore assessed the relationship between NIIs and transcriptional dysregulation in the R6/2 mouse, using double-label in situ hybridization combined with immunohistochemistry, and laser capture microdissection combined with quantitative real-time PCR. There was no difference in transcript levels of specific genes between NII-positive and NII-negative neurons. These results demonstrate that NIIs do not cause decreases in D2, PPE and PSS mRNA levels in R6/2 striatum and therefore are not involved in the down-regulation of these specific genes in this HD model. In addition, these observations argue against the notion that NIIs protect against transcriptional dysregulation in HD.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Down-Regulation
  • Enkephalins / genetics
  • Enkephalins / metabolism
  • Gene Expression Regulation*
  • Humans
  • Huntingtin Protein
  • Huntington Disease / genetics*
  • Huntington Disease / physiopathology
  • Immunohistochemistry
  • In Situ Hybridization
  • Intranuclear Inclusion Bodies / metabolism*
  • Mice
  • Mice, Transgenic
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neurons / cytology
  • Neurons / metabolism
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Protein Precursors / genetics
  • Protein Precursors / metabolism
  • Receptors, Dopamine D2 / genetics
  • Receptors, Dopamine D2 / metabolism
  • Somatostatin / genetics
  • Somatostatin / metabolism

Substances

  • Enkephalins
  • Htt protein, mouse
  • Huntingtin Protein
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • Protein Precursors
  • Receptors, Dopamine D2
  • Somatostatin
  • preproenkephalin