Analysis of supressive role of complement factors in prion propagation

2016 Fiscal Year Final Research Report

• Project/Area Number: 26450397
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Veterinary medical science
• Research Institution: Hokkaido University
• Principal Investigator: Hasebe Rie 北海道大学, 獣医学研究院, 講師 (70431335)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: プリオン病 / 補体因子 / 神経病態

Outline of Final Research Achievements

Roles of complement factors in neuropathogenesis of prion diseases are unknown. The results of the current study suggest that the amount of abnormal form of prion protein (PrPSc) was reduced in Chandler-infected primary cultured neurons, but was increased in 22L-infected neurons after temporary decrease. To assess the effects of complement reaction in in vivo prion infection, I injected lentivirus vectors harboring shRNA against complement factors C1qA and C3 into prion-infected mouse brains. In Chandler-infected mice, PrPSc was increased after C1q- and C3-shRNA injection. In contrast, PrPSc was decreased in 22L-infected mouse brains after C3-shRNA injection, but not C1qA-shRNA injection. These results suggest that the type and the effect of complement factors on the neuropathogenesis were different among the prion strains

Free Research Field

獣医病理学、病原微生物学