Journal
MICROBIOLOGY AND IMMUNOLOGY
Volume 58, Issue 7, Pages 361-374Publisher
WILEY
DOI: 10.1111/1348-0421.12162
Keywords
epilepsy; depression; neuroprotection; prion protein
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Funding
- Research Committee of Prion disease and Slow Virus Infection, the Ministry of Health, Labor and Welfare of Japan
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Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC-deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus-mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC-deficient mice reportedly have a more aggressive disease onset and less clinical improvement during the chronic phase than wild-type mice mice. In mice given oral dextran sulfate, PrPC has a potential protective role against inflammatory bowel disease. PrPC-deficient mice demonstrate significantly greater increases in blood glucose concentrations after intraperitoneal injection of glucose than wild-type mice. Further in vivo challenges to PrP gene-deficient models and conditional knockout models with siRNA and in vivo administration of PrP-ligating agents may assist in refining knowledge of the lymphoid function of PrPC and predicting the effects of anti-PrP treatment on the immune system. Together, these findings indicate that PrPC may have multiple neuroprotective and anti-inflammatory roles, which explains why this protein is so widely expressed.
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