摘要
目的探讨免疫相关GTP酶1(Irgml)在小鼠暂时性大脑中动脉缺血再灌注模型(tMCAO)中的表达及其对tMCAO小鼠大脑神经元内自噬发生的影响。方法采用westernblotting和免疫荧光染色,检测Irgml和自噬相关基因LC3I/II及P62在Irgml^+/+小鼠tMCAO脑组织内的表达水平及细胞定位;进一步比较Irgml^+/+及Irgml。小鼠tMCAO大脑神经元内自噬发生的差异。结果相比于假手术(sham)组,Irgml在Irgml^+/+小鼠tMCAO脑组织中表达明显增高,且主要分布于损伤侧皮层神经元内;同时我们也证实在小鼠tMCAO脑组织中LC3-II表达增加(t=-16.448,P〈0.01),而P62表达明显减低(t=3.975,P〈0.05)。我们进一步实验发现Irgml。小鼠tMCAO脑组织内LC3-II表达量低于Irgml^+/+小鼠tMCAO(t=4.073,P〈0.05),而P62表达量高于Irgml^+/+小鼠tMCAO(t=-3.383,P〈0.05)。结论在小鼠tMCAO模型中,Irgml参与调节大脑神经元的自噬活动。
Objective To investigate the impact of immunity-related GTPase Irgml on the regulation of neuronal autophagy in tMCAO mice. Methods Brain tissues were collected from lrgml +/+ tMCAO mice. Ir- gml and autophagy-related genes LC3- I / 11 and p62 expression were detected by western blotting and immu- nofluorescence staining. In addition, we compared the expression of autophagy related genes between the brain tissues of Irgm +/+ and Irgml -/- mice after tMCAO. Results Irgml was increased in the cortex neurons of Ir- gml +/+ mice tMCAO compared to sham group. The increatted Irgml was accompanied by enhanced neuronal autophagic activity proved by higher expression of LC3-II ( t = -16. 448, P 〈 0.01 ) and lower expression of p62 (t = 3. 975 ,P 〈 0.05) in Irgml +/+ mice tMCAO. However, we found that in Irgml -/- mice the exprossion of Lc3- II was lower ( P 〈 O. 01 ) while the expression of p62 was higher ( P 〈 0. 05 ) compared with that in Ir- gml +/+ mice. Conclusion The increased expression of Irgml in the neurons during tMCAO is important for neuronal autophagy.
出处
《国际免疫学杂志》
CAS
2012年第3期231-235,共5页
International Journal of Immunology
基金
黑龙江省教育厅海外学人科研资助重点项目(1153h08)