Relationship between the neural dysgenesis and increased production of class I MHC H-2Kk mRNA and protein in neurons of murine trisomy 16 fetuses

Biochem Biophys Res Commun. 1991 Aug 30;179(1):102-7. doi: 10.1016/0006-291x(91)91340-i.

Abstract

Neuronal cells from murine trisomy 16 fetuses have increased levels of class I MHC H-2Kk. To determine whether this increased level of H-2Kk protein product resulted from an increased synthesis of mRNA, a 33 base antisense cDNA probe complementary to a region in exon 2 of the H-2Kk sequence (nucleotide 392-424) was synthesized. This probe was used to examine, by in situ hybridization and immunohistochemistry, the neural distribution of H-2Kk mRNA and protein product. A marked elevation of the H-2Kk mRNA and protein were localized in mts16 neuronal populations that were susceptible to dysgenesis. The results implicate the expression of the H-2Kk in the neuropathology of mts16 and its human counterpart, Down syndrome.

MeSH terms

  • Animals
  • Brain / embryology
  • Brain / immunology*
  • Chromosome Mapping*
  • DNA Probes
  • Female
  • Fetus
  • Gestational Age
  • H-2 Antigens / genetics*
  • Histocompatibility Antigens Class I / genetics*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Neurons / immunology*
  • RNA, Messenger / genetics*
  • RNA, Messenger / metabolism
  • Translocation, Genetic
  • Trisomy*

Substances

  • DNA Probes
  • H-2 Antigens
  • H-2K(K) antigen
  • Histocompatibility Antigens Class I
  • RNA, Messenger