Lack of Alpha-Synuclein Modulates Microglial Phenotype In Vitro

被引：33

作者：

Austin, Susan A. ^{[1
]}

Rojanathammanee, Lalida ^{[1
]}

Golovko, Mikhail Y. ^{[1
]}

Murphy, Eric J. ^{[1
]}

Combs, Colin K. ^{[1
]}

机构：

[1] Univ N Dakota, Sch Med & Hlth Sci, Dept Pharmacol Physiol & Therapeut, Grand Forks, ND 58203 USA

来源：

NEUROCHEMICAL RESEARCH | 2011年 / 36卷 / 06期

基金：

美国国家卫生研究院; 美国国家科学基金会;

关键词：

Microglia; Phagocytosis; Cytokine; Parkinson; alpha-Synuclein; Phospholipase D; AMYLOID PRECURSOR PROTEIN; PHOSPHOLIPASE-D; PARKINSONS-DISEASE; ACTIVATES MICROGLIA; ACID INCORPORATION; PHOSPHATIDIC-ACID; PROSTAGLANDIN E-2; GENE-ABLATION; UP-REGULATION; CELLS;

D O I：

10.1007/s11064-011-0439-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Alpha (alpha)-synuclein neuronal effects are continually being defined although its role in regulating glial phenotypes remains unclear. An ability to regulate microglial activation was investigated using primary cultures from wild type and alpha-synuclein deficient mice (Snca (-/-)). Snca (-/-) microglia demonstrated increased secretion of the cytokine tumor necrosis factor-alpha (TNF-alpha), impaired phagocytic ability, elevated prostaglandin levels, and increased protein levels of key enzymes in lipid-mediated signaling events, cytosolic phospholipase (cPLA(2)), cyclooxygenase-2 (Cox-2) and phospholipase D2 (PLD2) when compared to wild type cells. Increased cytokine secretion and cPLA(2) and Cox-2 levels in Snca (-/-) microglia were partially attenuated by inhibiting PLD-dependent signaling with n-butanol treatment.

引用

页码：994 / 1004

页数：11

共 76 条

[1]

A-synuclein interacts with phospholipase D isozymes and inhibits pervanadate-induced phospholipase D activation in human embryonic kidney-293 cells [J].