当前位置: 首页 > 文章 > PrP106-126诱导的N2a细胞神经毒性中神经营养因子受体p75~(NTR)的表达变化研究 畜牧兽医学报 2009,40 (3) 416-420
Position: Home > Articles > Altered Expression of Neurotrophin Receptor p75~(NTR) in PrP106-126-induced Neurotoxicity of N2a cells Chinese Journal of Animal and Veterinary Sciences 2009,40 (3) 416-420

PrP106-126诱导的N2a细胞神经毒性中神经营养因子受体p75~(NTR)的表达变化研究

作  者:
白瑜;李玉荣;周向梅;尹晓敏;赵德明
单  位:
河北农业大学动物科技学院;中国农业大学动物医学院
关键词:
朊病毒;PrP106-126;p75NTR;神经毒性;小鼠成神经瘤细胞N2a
摘  要:
神经元死亡是朊病毒病的主要病理学特征。朊蛋白多肽PrP106-126能够对神经细胞表现神经毒性,引起细胞凋亡。细胞表面蛋白神经营养因子受体p75NTR的胞外区域可以与PrP106-126结合并产生促凋亡作用。作者以小鼠成神经瘤细胞N2a为细胞模型,应用荧光定量RT-PCR和Western Blot技术,以及DNA Ladder和AnnexinV-FITC/PI双重染色流式细胞凋亡检测技术对p75NTR介导的PrP106-126神经毒性分子机制进行了研究。结果发现在PrP106-126诱导的N2a细胞凋亡过程中,p75NTR的mRNA转录水平和蛋白表达水平均显著升高,以p75NTR多克隆抗体sc-6189阻断PrP 106-126与p75NTR的相互作用后,减弱了PrP106-126诱导的N2a细胞凋亡效果。该研究揭示了PrP106-126诱导的N2a细胞毒性中p75NTR受体的表达变化,为解释朊病毒病的发病机制提供了重要数据。
译  名:
Altered Expression of Neurotrophin Receptor p75~(NTR) in PrP106-126-induced Neurotoxicity of N2a cells
作  者:
BAI Yu1,LI Yu-rong1,2,ZHOU Xiang-mei1,YIN Xiao-min1,ZHAO De-ming1* (1.National Animal TSE Laboratory,College of Veterinary Medicine,China Agricultural University,Beijing 100193,China;2.College of Animal Science and Technology,Agricultural University of Hebei,Baoding 071001,China)
关键词:
prion;PrP106-126;p75NTR;neurotoxicity;mouse neuroblastoma cells N2a
摘  要:
Neuronal death is a pathological hallmark of prion diseases.Synthetic prion peptide PrP106-126 can cause neurotoxicity and induce apoptosis in neuronal cells.Extracellular region of neurotrophin receptor p75NTR,a cell surface protein,could bind to PrP106-126 and has apoptotic effect on neurons.Using quantitative RT-PCR,Western Blot technique,DNA Ladder assay,and flow cytometry(FCM) assay with Annexin V-FITC/PI double-stained,we investigated the p75NTR-mediated neurotoxicity by PrP106-126 in mouse neuroblastoma cells N2a.The results showed that in PrP106-126-induced apoptosis of N2a cells,p75NTR expression was significantly up-regulated at mRNA and protein levels,and blocking the interaction of p75NTR with PrP 106-126 by p75NTR polyclone antibody sc-6189 attenuated the apoptotic effect induced by PrP106-126.This study showed that mRNA and protein expression of receptor p75NTR were altered in PrP106-126-induced neurotoxicity of N2a cells,and this may partially account for the pathogenesis of prion disease.

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