Expression and secretion of apoE isoforms in astrocytes and microglia during inflammation

小胶质细胞 载脂蛋白E 生物 神经科学 炎症 分泌物 星形胶质细胞 细胞生物学 神经胶质 基因亚型 免疫学 内分泌学 内科学 中枢神经系统 基因 医学 生物化学 疾病
作者
Maria Fe Lanfranco,Jordy Sepulveda,Gregory Kopetsky,G. William Rebeck
出处
期刊:Glia [Wiley]
卷期号:69 (6): 1478-1493 被引量:95
标识
DOI:10.1002/glia.23974
摘要

Abstract Neuroinflammation is a common feature in neurodegenerative diseases, modulated by the Alzheimer's disease risk factor, apolipoprotein E ( APOE ). In the brain, apoE protein is synthesized by astrocytes and microglia. We examined primary cultures of astrocytes and microglia from human APOE (E2 , E3 , and E4) targeted‐replacement mice. Astrocytes secreted two species of apoE, whereas cellular apoE consisted of only one. Both forms of secreted astrocytic apoE were bound during glycoprotein isolation, and enzymatic removal of glycans produced a convergence of the two forms of apoE to a single form; thus, the two species of astrocyte‐secreted apoE are differentially glycosylated. Microglia released only a single species of apoE, while cellular apoE consisted of two forms; the secreted apoE and one of the two forms of cellular apoE were glycosylated. We treated the primary glia with either endogenous (TNFα) or exogenous (LPS) pro‐inflammatory stimuli. While LPS had no effect on astrocytic apoE, APOE2 , and APOE3 microglia increased release of apoE; APOE4 microglia showed no effect. APOE4 microglia showed higher baseline secretion of TNFα compared to APOE2 and APOE3 microglia. TNFα treatment reduced the secretion and cellular expression of apoE only in APOE4 astrocytes. The patterns of apoE species produced by astrocytes and microglia were not affected by inflammation. No changes in APOE mRNA were observed in astrocytes after both treatments. Together, our data demonstrate that astrocytes and microglia differentially express and secrete glycosylated forms of apoE and that APOE4 astrocytes and microglia are deficient in immunomodulation compared to APOE2 and APOE3 .
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
cetomacrogol完成签到,获得积分10
2秒前
陈功发布了新的文献求助10
3秒前
隐形曼青应助鱼咬羊采纳,获得10
3秒前
yanshapo完成签到,获得积分10
4秒前
4秒前
坤坤发布了新的文献求助10
4秒前
土豆炖大锅完成签到,获得积分10
5秒前
酷波er应助Andorchid采纳,获得10
5秒前
muyassar发布了新的文献求助10
5秒前
大气的画板完成签到,获得积分10
6秒前
6秒前
fenghp发布了新的文献求助10
6秒前
8秒前
奥利奥发布了新的文献求助10
8秒前
LLL完成签到,获得积分10
8秒前
9秒前
9秒前
9秒前
10秒前
12秒前
毛豆应助yelv123采纳,获得10
12秒前
谦让小玉完成签到,获得积分10
12秒前
12秒前
周凡淇发布了新的文献求助10
12秒前
伶俐皮卡丘完成签到,获得积分20
12秒前
12秒前
12秒前
背后的世开完成签到,获得积分20
13秒前
momo发布了新的文献求助10
13秒前
LLL发布了新的文献求助10
13秒前
鱼咬羊完成签到,获得积分10
13秒前
有米饭没完成签到 ,获得积分10
13秒前
14秒前
14秒前
香蕉觅云应助奥利奥采纳,获得10
15秒前
15秒前
兰瓜瓜完成签到,获得积分10
16秒前
16秒前
16秒前
高分求助中
Continuum Thermodynamics and Material Modelling 3000
Production Logging: Theoretical and Interpretive Elements 2700
Les Mantodea de Guyane Insecta, Polyneoptera 1000
Structural Load Modelling and Combination for Performance and Safety Evaluation 1000
Conference Record, IAS Annual Meeting 1977 720
電気学会論文誌D(産業応用部門誌), 141 巻, 11 号 510
有源雷达散射截面减缩——理论与应用 赫玛·辛格,拉凯什·莫汉·杰哈 500
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 基因 遗传学 物理化学 催化作用 量子力学 光电子学 冶金
热门帖子
关注 科研通微信公众号,转发送积分 3569139
求助须知:如何正确求助?哪些是违规求助? 3140579
关于积分的说明 9438103
捐赠科研通 2841578
什么是DOI,文献DOI怎么找? 1561750
邀请新用户注册赠送积分活动 730628
科研通“疑难数据库(出版商)”最低求助积分说明 718167