Cellular prion protein prevents brain damage after encephalomyocarditis virus infection in mice.
Cellular prion protein (PrP(C)), a cell-surface glycoprotein normally associated with neurons, is also expressed in other cell types such as glia and lymphocytes. To further elucidate these roles of PrP(C), wild-type prion protein gene (Prnp(+/+)) mice and Prnp-deficient (Prnp(-/-)) mice were infected with encephalomyocarditis virus B variant (EMCV-B) via an intracranial route. EMCV-B causes encephalitis and apoptotic cell death in vivo. Histopathological studies revealed that Prnp(+/+) mice infected with 600 pfu of EMCV-B showed more severe infiltration of inflammatory cells, accompanied by higher activation of microglia cells around the hippocampus, than Prnp(-/-) mice; viz., no differences in the brain virus titer between these two lines of mice. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP, nick end-labeling (TUNEL) staining of the brain specimens revealed that the CA1 hippocampal pyramidal cells showed a larger number of apoptotic neurons in Prnp(-/-) than Prnp(+/+) mice. Based on all these findings, PrP(C) may play certain roles in the induction of inflammation and inhibition of apoptosis in vivo.
Nasu-Nishimura
Y
Y
Department of Molecular Immunology, School of Agricultural and Life Sciences, University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan.
Taniuchi
Y
Y
Nishimura
T
T
Sakudo
A
A
Nakajima
K
K
Ano
Y
Y
Sugiura
K
K
Sakaguchi
S
S
Itohara
S
S
Onodera
T
T
D000818:Animals; D017209:Apoptosis; D018188:Cardiovirus Infections / Q000473:pathology* / Q000821:virology; D002452:Cell Count; D004686:Encephalomyocarditis virus; D006624:Hippocampus / Q000473:pathology; D007249:Inflammation / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D017628:Microglia / Q000473:pathology; D018621:PrPC Proteins / Q000502:physiology*; D011328:Prions / Q000235:genetics; D017966:Pyramidal Cells / Q000166:cytology / Q000502:physiology
D018621:PrPC Proteins; D011328:Prions