CRMP-2 is involved in hypoxic preconditioning-induced neuroprotection against cerebral ischemic injuries of mice
- VernacularTitle:脑衰蛋白反应调节蛋白-2参与低氧预适应减轻小鼠脑缺血损伤
- Author:
Caiyan ZHANG
;
Sujuan FENG
;
Xu LIU
;
Xiangning BU
;
Nan ZHANG
;
Yaxin ZHENG
;
Xiaowen YUAN
;
Xiaoguang LI
;
Junfa LI
- Publication Type:Journal Article
- Keywords:
cPKCβⅡ;
collapsin response mediator protein-2 ( CRMP-2);
proteomics;
hypoxic preconditioning ( HPC);
middle cerebral artery occlusion (MCAO)
- From:
Basic & Clinical Medicine
2009;29(11):1133-1138
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether conventional protein kinase C (cPKC ) βⅡ-interacting collapsin response mediator protein-2 (CRMP-2) provides neuroprotection against cerebral ischemic (I) injuries. Methods Male BALB/c mice were randomly divided into normoxic control (Nor) , HPC, Nor + Sham, HPC + Sham, Nor + I and HPC + I groups (n = 6 per group). Using our HPC and MCAO mouse models, we applied immunoprecipita-tion, two-dimensional electrophoresis and mass spectrometry to characterize cPKCβⅡ-interacting proteins and combined with SDS-PAGE and Western blot to quantitatively analyze CRMP-2 phosphorylation and degradation levels in the brain of mice after HPC and MCAO. Results The expression level of 10 cPKCβⅡ-interacting proteins changed obviously in cerebral cortex of HPC mice when compared with Nor group. One of these proteins, CRMP-2 protein level increased in particulate fraction and decreased in cytosolic fraction of cerebral cortex of HPC mice. CRMP-2 phosphorylation level in ischemic core (Ic) of cerebral cortex decreased significantly ( P < 0. 05 , n = 6) as compared with that of Nor + sham group, but CRMP-2 phosphorylation level in HPC +I group increased significantly as compared with that of Nor +I group ( P < 0. 05, n = 6). In ischemic cortex, CRMP-2 degradation (proteolysis) was observed as the appearance of 55 ku breakdown products (BDP). However, the CRMP-2 degradation level, BDPs products decreased significantly in penumbra ( P) of ischemic cortex from HPC +I group when we compared with that of Nor +I group (P < 0. 05, n = 6 ). Conclusion CRMP-2 is involved in attenuating the decrease of CRMP-2 phosphorylation in ischemic core and in inhibiting its degradation in penumbra of cerebral cortex of mice thereby to lessen the ischemic injuries.
