Alterations of CaM pathway in the brains of scrapie infected mice
10.3760/cma.j.issn.1003-9279.2017.01.003
- VernacularTitle: 羊瘙痒因子139A感染小鼠脑组织中CaM信号通路变化的研究
- Author:
Renqing ZHANG
1
,
2
;
Jing SUN
3
;
Yue MA
3
;
Xiaodong YANG
3
;
Yan LYU
3
;
Xiaofeng XU
3
;
Zhibao CHEN
1
;
Xiaoping DONG
3
;
Lijie XIAO
1
;
Cao CHEN
3
Author Information
1. College of Life Science and Technology, Heilongjiang Bayi Agriculture University, Daqing 163000, China
2. National Institute for Viral Disease Control and Prevention, State Key Laboratory for Communicable Disease Prevention and Control, Chinese Center for Disease Control and Prevention, Beijing 102206, China
3. National Institute for Viral Disease Control and Prevention, State Key Laboratory for Communicable Disease Prevention and Control, Chinese Center for Disease Control and Prevention, Beijing 102206, China
- Publication Type:Journal Article
- Keywords:
Prion diseases;
Calmodulin;
Ca2+ /Calmodulin-dependent binding protein
- From:
Chinese Journal of Experimental and Clinical Virology
2017;31(1):13-17
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To analysis the alterations of CaM and its downstream factors in the brains of scrapie infected mice.
Methods:Using the methods of Western blot and immunohistochemistry assay to detect the levels and distributions of CaM, as well as the expressing alterations of the downstream substrates of CaM in the brains of mice infected with scrapie.
Results:Compared with the normal controls, the levels of CaM are significantly increased in the brains of scrapie-infected mice and particularly distributing in the regions of cortex, thamalus and cerebellum. Remarkable high levels of CaMKII, p-CaMKII and p-CaMKIV are observed in the brain homogenates of scrapie-infected mice. The regulatory protein of cAMP response element binding protein (CREB) and p-CERB are also increased, while the levels of BDNF which is regulated by p-CREB are obeviously downregulated.
Conclusions:The synthesis of BDNF may be influenced by the prion replication in neuron and further attenuates its neuronal protective features.
