Identification of macrophage/microglia activation factor (MAF) associated with late endosomes/lysosomes in microglial cells
Identification of macrophage/microglia activation factor (MAF) associated with late endosomes/lysosomes in microglial cells
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DOI：
10.1016/s0014-5793(04)00244-3
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发表时间：
2004-04-09
期刊：
影响因子：
3.5
通讯作者：
Savaskan, NE
中科院分区：
文献类型：
--
作者：
Bräuer, AU;Nitsch, R;Savaskan, NE
对中枢神经系统的损伤触发神经胶质细胞向病变部位的快速活化和特异性迁移。在那里，神经胶质细胞对损伤后发生的继发性神经元变化有很大贡献。在试图确定脑外伤后胶质细胞激活的分子线索，我们进行了差异显示逆转录-聚合酶链反应筛选损伤和对照海马。在这里，我们报告的巨噬细胞/小胶质细胞活化因子（MAY），一个新的膜蛋白与7个推定的跨膜结构域的鉴定。表达分析显示MAF主要在脑中的小胶质细胞中表达，并且在脑损伤后上调。MAY在非神经胶质细胞中的过表达显示与溶酶体标志物内体/溶酶体相关膜蛋白-1（lamp-1）的细胞内共分布。此外，MAF转染的细胞显示MAY主要与晚期内体/溶酶体相关，并且这种关联可以通过激活蛋白激酶C依赖性途径来破坏。总之，这些结果意味着MAF参与了与脑损伤后小胶质细胞活化相关的溶酶体膜的动力学。(C)2004年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
Damage to the central nervous system triggers rapid activation and specific migration of glial cells towards the lesion site. There, glial cells contribute heavily to secondary neuronal changes that take place after lesion. In an attempt to identify the molecular cues of glial activation following brain trauma we performed differential display reverse transcription-polymerase chain reaction screenings from lesioned and control hippocampus . Here we report on the identification of the macrophage/microglia activation factor (MAY), a new membrane protein with seven putative transmembrane domains. Expression analysis revealed that MAF is predominantly expressed in microglial cells in the brain, and is upregulated following brain lesion. Overexpression of MAY in non-glial cells shows an intracellular codistribution with the lysosomal marker endosome/lysosome-associated membrane protein-1 (lamp-1). Furthermore, MAF-transfected cells show that MAY is primarily associated with late endosomes/lysosomes, and that this association can be disrupted by activation of protein kinase C-dependent pathways. In conclusion, these results imply that MAF is involved in the dynamics of lysosomal membranes associated with microglial activation following brain lesion. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.