Correlation of increased levels of class I MHC H-2Kk in the placenta of murine trisomy 16 conceptuses with structural abnormalities revealed by magnetic resonance microscopy

Authors

  • Steven Kornguth,

    Corresponding author
    1. Department of Neurology, University of Wisconsin–Madison, Madison, Wisconsin 53705
    2. Department of Physiological Chemistry, University of Wisconsin–Madison, Madison, Wisconsin 53705
    • Rm 659, Waisman Center, Departments of Neurology and Physiological Chemistry, University of Wisconsin–Madison, Madison, WI 53705
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  • Edward Bersu,

    1. Department of Anatomy, University of Wisconsin–Madison, Madison, Wisconsin 53705
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  • Mark Anderson,

    1. Department of Biochemistry, University of Wisconsin–Madison, Madison, Wisconsin 53705
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  • John Markley

    1. Department of Anatomy, University of Wisconsin–Madison, Madison, Wisconsin 53705
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Abstract

Murine trisomy 16 (mts16) placentas and fetuses, 17-day gestation age, were examined histologically and by magnetic resonance imaging at 9.4 T and compared with control littermate tissues. Placentas were studied by immunohistochemical methods, at 15-days gestational age, for expression of the major histocompatibility complex (MHC) class I H-2Kk cell surface marker. Immunohistochemical studies revealed a markedly increased expression of the MHC marker H-2Kk on cells in the labyrinth of the placenta of mts16. There were differences between the magnetic resonance (MR) images of the trisomic and normal placentas, which may be correlated with the increased expression of H-2Kk in the mts16 placental labyrinth. The decidual and labyrinthine components of the normal placentas showed similar high signal intensities (SI) while in trisomic placentas a marked high SI was characteristic only of the decidual region on proton spin density images. The MRI also revealed a smaller cerebellum in the ts16 fetuses. The potential effects of the compromised structure of the placental labyrinth and the overexpression of the H-2Kk marker on the mts16 neural and placental dysgenesis are discussed.

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