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The murine microglial cell line BV2 has neuroprotective effects, but is toxic to neurons by secret-ing inlfammatory cytokines, and is an important target in the treatment of nerve inlfammation 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 ex-pression. 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.
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miR-195保护大鼠慢性脑低灌注诱发痴呆的作用与APLP2的关系
目的 研究miR-195在大鼠慢性脑低灌注诱发痴呆中的作用与APLP2的关系,为痴呆的诊断和治疗提供实验依据.方法 采用双侧颈总动脉结扎法(bilateral common carotid arteries occlusion,2VO)建立大鼠血管性痴呆模型;通过Western blot法检测血管性痴呆鼠脑组织中淀粉样肽前体样蛋白(amyloid precursor like protein,APLP2)的表达.同时在体脑立体定位注射miR-195、antisense oligoridonucleopides(AMO)-miR-195慢病毒表达载体.结果 大鼠大脑低灌注后海马及皮层组织APLP2表达无明显变化;脑立体定位注射AMO-miR-195慢病毒载体对APLP2表达无明显影响;2VO大鼠脑立体定位注射miR-195慢病毒载体对APLP2的表达无明显影响.结论 miR-195保护大鼠慢性脑低灌注诱发痴呆中的作用与APLP2无关.
