Li Guangzhe, Chen Hui, Cheng Lin, Zhao Rongjie, Zhao Junchang, Xu Yanji
Department of Psychology, Yanbian Brain Hospital, Yanji, Jilin Province, China.
Department of Preventive Medicine, Medical College, Yanbian University, Yanji, Jilin Province, China.
Neural Regen Res. 2014 Nov 1;9(21):1923-8. doi: 10.4103/1673-5374.145362.
The murine microglial cell line BV2 has neuroprotective effects, but is toxic to neurons by secreting inflammatory cytokines, and is an important target in the treatment of nerve inflammation and neurodegenerative diseases. In the present study, we observed the effects of transfecting three amyloid precursor-like protein 2 (APLP2) C-terminal fragments (CTFs; C57, C50 and C31) in the pEGFP-N1 vector on S100A9 expression in BV2 cells. Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector. Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression. Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer's disease.
小鼠小胶质细胞系BV2具有神经保护作用，但通过分泌炎性细胞因子对神经元有毒性，是治疗神经炎症和神经退行性疾病的重要靶点。在本研究中，我们观察了在pEGFP-N1载体中转入三个淀粉样前体样蛋白2（APLP2）C末端片段（CTF；C57、C50和C31）对BV2细胞中S100A9表达的影响。逆转录PCR、蛋白质印迹分析和免疫细胞化学显示，与用空载体进行模拟转染相比，CTF转染后BV2细胞中S100A9蛋白和mRNA表达更高。此外，全长APLP2-751转染导致S100A9蛋白表达水平较低。我们的结果表明，APLP2-CTF上调BV2细胞中S100A9蛋白和mRNA表达，并确定了一条参与阿尔茨海默病中神经元损伤、凋亡以及修复和保护的新途径。
