Increased expression of glial fibrillary acidic protein fragments and mu-calpain activation within the hippocampus of prion-infected mice
Increased expression of glial fibrillary acidic protein fragments and mu-calpain activation within the hippocampus of prion-infected mice
Prion diseases are characteristically accompanied by marked astrocytic activation, which is initiated relatively early in the disease process. Using the intracerebrally injected ME7 strain of prion agent to model disease, we identified an expected increase in GFAP (glial fibrillary acidic protein) but additionally noted an accumulation of GFAP cleavage fragments in hippocampal homogenates. A time-dependent increase in hippocampal m-calpain immunoreactivity within astrocytes suggests that its proteolytic activity may account for the cleavage of GFAP that is observed in the ME7 model. It may therefore contribute to the reactive gliosis that is characteristic of prion diseases.
m-calpain, central nervous system, glial fibrillary acidic protein, gliosis, ME7, prion disease
51-54
Gray, B.C.
a244fdd1-41ec-4d1a-866f-ef6ec93e18da
Skipp, P.
1ba7dcf6-9fe7-4b5c-a9d0-e32ed7f42aa5
Connor, V.M.
3f8d700b-28e0-4444-904e-bd7bded0e3f6
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
1 February 2006
Gray, B.C.
a244fdd1-41ec-4d1a-866f-ef6ec93e18da
Skipp, P.
1ba7dcf6-9fe7-4b5c-a9d0-e32ed7f42aa5
Connor, V.M.
3f8d700b-28e0-4444-904e-bd7bded0e3f6
Perry, V.H.
8f29d36a-8e1f-4082-8700-09483bbaeae4
Gray, B.C., Skipp, P., Connor, V.M. and Perry, V.H.
(2006)
Increased expression of glial fibrillary acidic protein fragments and mu-calpain activation within the hippocampus of prion-infected mice.
Biochemical Society Transactions, 34 (1), .
Abstract
Prion diseases are characteristically accompanied by marked astrocytic activation, which is initiated relatively early in the disease process. Using the intracerebrally injected ME7 strain of prion agent to model disease, we identified an expected increase in GFAP (glial fibrillary acidic protein) but additionally noted an accumulation of GFAP cleavage fragments in hippocampal homogenates. A time-dependent increase in hippocampal m-calpain immunoreactivity within astrocytes suggests that its proteolytic activity may account for the cleavage of GFAP that is observed in the ME7 model. It may therefore contribute to the reactive gliosis that is characteristic of prion diseases.
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Published date: 1 February 2006
Keywords:
m-calpain, central nervous system, glial fibrillary acidic protein, gliosis, ME7, prion disease
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Local EPrints ID: 56708
URI: http://eprints.soton.ac.uk/id/eprint/56708
ISSN: 0300-5127
PURE UUID: cf7b6262-bf0a-40e3-9ab4-a2de2913fc8e
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Date deposited: 06 Aug 2008
Last modified: 28 Apr 2022 01:36
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Author:
B.C. Gray
Author:
V.M. Connor
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