Abnormal Activation of Glial Cells in the Brains of Prion Protein-deficient Mice Ectopically Expressing Prion Protein-like Protein, PrPLP/Dpl View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2001-12-01

AUTHORS

Ryuichiro Atarashi, Suehiro Sakaguchi, Kazuto Shigematsu, Kazuhiko Arima, Nobuhiko Okimura, Naohiro Yamaguchi, Aimin Li, Juraj Kopacek, Shigeru Katamine

ABSTRACT

BackgroundSome lines of mice homozygous for a disrupted prion protein gene (Prnp), including Ngsk Prnp0/0 mice, exhibit Purkinje cell degeneration as a consequence of the ectopic overexpression of the downstream gene for prion protein-like protein (PrPLP/Dpl) in the brain, but others, such as Zrch I Prnp0/0 mice, show neither the neurodegeneration nor the expression of PrPLP/Dpl. In the present study, we found that Ngsk Prnp0/0, but not Zrch I Prnp0/0 mice, developed gliosis involving both astrocytes and microglia in the brain.Materials and MethodsThe brains from wild-type (Prnp+/+), Ngsk Prnp0/0, Zrch I Prnp0/0, and reconstituted Ngsk Prnp0/0 mice carrying a mouse PrP transgene, designated Tg(P) Ngsk Prnp0/0 mice, were subjected into Northern blotting and in situ hybridization using probes of glial fibrillary acidic protein (GFAP) and lysozyme M (LM) specific for astrocytes and microglia, respectively. Immunohistochemistry was also performed on the brain sections using anti-GFAP and anti-F4/80 antibodies.ResultsNorthern blotting demonstrated upregulated expression of the genes for GFAP and LM in the brains of Ngsk Prnp0/0, but not in Zrch I Prnp0/0 mice. A transgene for normal mouse PrPC successfully rescued Ngsk Prnp0/0 mice from the glial activation. In situ hybridization and immunohistochemistry revealed activated astrocytes and microglia mainly in the white matter of both the forebrains and cerebella. In contrast, there was no evidence of neuronal injury except for the Purkinje cell degeneration. Moreover, the glial cell activation was notable well before the onset of the Purkinje cell degeneration.ConclusionsThese findings strongly suggest that ectopic PrPLP/Dpl in the absence of PrPC is actively involved in the glial-cell activation in the brain. More... »

PAGES

803-809

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf03401972

DOI

http://dx.doi.org/10.1007/bf03401972

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1074998370

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11844868


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32 schema:description BackgroundSome lines of mice homozygous for a disrupted prion protein gene (Prnp), including Ngsk Prnp0/0 mice, exhibit Purkinje cell degeneration as a consequence of the ectopic overexpression of the downstream gene for prion protein-like protein (PrPLP/Dpl) in the brain, but others, such as Zrch I Prnp0/0 mice, show neither the neurodegeneration nor the expression of PrPLP/Dpl. In the present study, we found that Ngsk Prnp0/0, but not Zrch I Prnp0/0 mice, developed gliosis involving both astrocytes and microglia in the brain.Materials and MethodsThe brains from wild-type (Prnp+/+), Ngsk Prnp0/0, Zrch I Prnp0/0, and reconstituted Ngsk Prnp0/0 mice carrying a mouse PrP transgene, designated Tg(P) Ngsk Prnp0/0 mice, were subjected into Northern blotting and in situ hybridization using probes of glial fibrillary acidic protein (GFAP) and lysozyme M (LM) specific for astrocytes and microglia, respectively. Immunohistochemistry was also performed on the brain sections using anti-GFAP and anti-F4/80 antibodies.ResultsNorthern blotting demonstrated upregulated expression of the genes for GFAP and LM in the brains of Ngsk Prnp0/0, but not in Zrch I Prnp0/0 mice. A transgene for normal mouse PrPC successfully rescued Ngsk Prnp0/0 mice from the glial activation. In situ hybridization and immunohistochemistry revealed activated astrocytes and microglia mainly in the white matter of both the forebrains and cerebella. In contrast, there was no evidence of neuronal injury except for the Purkinje cell degeneration. Moreover, the glial cell activation was notable well before the onset of the Purkinje cell degeneration.ConclusionsThese findings strongly suggest that ectopic PrPLP/Dpl in the absence of PrPC is actively involved in the glial-cell activation in the brain.
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40 ConclusionsThese findings
41 DPL
42 Expressing Prion Protein-like Protein
43 I Prnp0/0
44 I Prnp0/0 mice
45 MethodsThe brains
46 Ngsk Prnp0/0
47 Ngsk Prnp0/0 mice
48 Northern blotting
49 PrP transgenes
50 PrPC
51 PrPLP/Dpl
52 Prnp0/0
53 Prnp0/0 mice
54 Purkinje cell degeneration
55 Zrch I Prnp0/0
56 Zrch I Prnp0/0 mice
57 abnormal activation
58 absence
59 absence of PrPC
60 acidic protein
61 activated astrocytes
62 activation
63 anti-F4/80 antibody
64 antibodies
65 astrocytes
66 blotting
67 brain
68 brain sections
69 cell activation
70 cell degeneration
71 cells
72 cerebellum
73 consequences
74 contrast
75 degeneration
76 developed gliosis
77 downstream genes
78 ectopic PrPLP/Dpl
79 ectopic overexpression
80 evidence
81 exhibit Purkinje cell degeneration
82 expression
83 fibrillary acidic protein
84 findings
85 forebrain
86 genes
87 glial activation
88 glial cell activation
89 glial cells
90 glial fibrillary acidic protein
91 glial-cell activation
92 gliosis
93 hybridization
94 immunohistochemistry
95 injury
96 lines
97 lysozyme M
98 materials
99 matter
100 mice
101 microglia
102 mouse PrP transgene
103 mouse PrPC
104 neurodegeneration
105 neuronal injury
106 normal mouse PrPC
107 onset
108 overexpression
109 present study
110 prion protein gene
111 prion protein-deficient mice
112 prion protein-like protein
113 probe
114 protein
115 protein gene
116 protein-deficient mice
117 protein-like protein
118 sections
119 situ hybridization
120 study
121 transgene
122 upregulated expression
123 white matter
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