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Molecular analysis of prion protein (PrP) and glial fibrillary acidic protein (GFAP) transcripts in experimental Creutzfeldt Jakob disease in mice

100%
Kordek R., Liberski P. P., Yanagihra R., Isaacson S., Gajdusek D. C.
Acta Neurobiologiae Experimentalis
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1997
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vol. 57
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issue 2
85-90
EN
Prion protein (PrPsc) which accumulates in the brains affected with subacute spongiform encephalopathies (SSE) is altered isoform of normal, cellular isoform (PrPc), and PrP deposition is accompanied with spongiosis and astrogliosis. To find the amounts of PrP and GFAP transcripts during progression of experimental Creutzfeldt Jakob disease we performed comparative RT PCR on the terminally sick mice brains, 22 weeks following inoculation with Fujisaki strain of CJD agent, and on control brains. The intensity of bands for PrP mRNA and control beta actin were similar for infected and uninfected brains, while amounts of transcripts for GFAP increased as for cytokines released by glial cells TNF-alpha and IL-1 alpha. This study supports thesis that PrPc to PrPsc conversion is post translational process not related to PrP overproduction. Increased amounts of GFAP mRNA during the course of the disease correlated with astrocytosis estimated by immunohistochemistry with anti GFAP antibody.
2
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Difluoromethylornithine counteracts lesion-induced astrogliosis in rat hippocampus: enhancement of inhibitory effect by combined treatment with GM1 ganglioside

61%
Jaglinski W., Skup M., Zaremba M., Oderfeld-Nowak B.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
549-553
EN
The effect of difluoromethylornithine (DFMO), an irrevesible inhibitor of ornithine decarboxylase (ODC), the rate limiting enzyme of polyamine biosynthesis, and its combined action with GM1 ganglioside, was studied on the GFAP content in a model of remote astrogliosis evoked in the hippocampus by latral fimbria transection.DFMO markedly suppressed hipocampal gliosis as measured by GFAP immunoblotting seven days postsurgery.Combined treatment with DFMO and GM1 ganglioside produced a stronger suppressive effect than DFMO.The results support the hypothesis of a causal link between lesion induced events:polyamine biosynthesis and astroglial reaction.Potentation of the inhibitory effect of DFMO by GM1 ganglioside suggest that the latter does not act through the mechanism involving ODC suppression.
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