Intrinsic expression of transcortin in neural cells of the mouse brain: a histochemical and molecular study.

Elena Sivukhina, Jean-Christophe Helbling, Amandine M. Minni, H. Hendrik Schäfer, Véronique Pallet, Gustav F. Jirikowski, Marie-Pierre Moisan
J Exp Biol. 2012-09-20; 216(2): 245-252
DOI: 10.1242/jeb.076893

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Corticosteroid binding globulin (CBG, transcortin) has been shown to be expressed
in the brain of rat and human species. In this study, we examined the CBG brain
expression and cDNA structure in mice, comparing wild-type (Cbg(+/+)) and Cbg
knockout mice (Cbg(-/-), obtained by genetic disruption of the SerpinA6 alias Cbg
gene). We used double immunofluorescence labeling with specific neuronal and
glial markers to analyze the cellular localization of CBG in various regions of
the mouse brain. In wild-type (Cbg(+/+)) mice, we found CBG immunoreactivity in
neuronal perikarya of the magnocellular hypothalamic nuclei, amygdala,
hippocampus, cerebral cortex, cerebellum and pituitary. A portion of glial cells
(astrocytes, oligodendrocytes) contained CBG immunoreactivity, including some of
the ependymal cells and choroid plexus cells. No CBG immunoreactivity was
detected in Cbg(-/-) brain tissues. Using RT-PCR, we showed that the full-length
Cbg mRNA is present in those regions, indicating an intrinsic expression of the
steroid-binding globulin. Furthermore, sequencing analysis showed that Cbg cDNA
obtained from the mouse hypothalamus was homologous to Cbg cDNA obtained from the
liver. Finally, we have evaluated the relative levels of CBG expression in
various brain regions and in the liver by quantitative PCR. We found that brain
levels of Cbg mRNA are low compared with the liver but significantly higher than
in CBG-deficient mice. Although derived from the same gene as liver CBG, brain
CBG protein may play a specific or complementary role that requires the
production and analysis of brain-specific Cbg knockout models.


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