Molecular mechanisms of signaling via the docosanoid neuroprotectin D1 for cellular homeostasis and neuroprotection

被引：75

作者：

Asatryan, Aram ^{[1
]}

Bazan, Nicolas G. ^{[1
]}

机构：

[1] Louisiana State Univ Hlth New Orleans, Sch Med, Neurosci Ctr Excellence, 2020 Gravier St, New Orleans, LA 70112 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2017年 / 292卷 / 30期

基金：

美国国家卫生研究院;

关键词：

cell death; lipid signaling; neurodegenerative disease; NF-kB transcription factor; retina; NF-KAPPA-B; NECROSIS-FACTOR-ALPHA; PROLIFERATOR-ACTIVATED RECEPTORS; PIGMENT EPITHELIAL-CELLS; DOCOSAHEXAENOIC ACID; C-REL; TRANSCRIPTION FACTOR; OXIDATIVE STRESS; OXIDIZED OMEGA-3-FATTY-ACIDS; GENE-EXPRESSION;

D O I：

10.1074/jbc.R117.783076

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Docosahexaenoic acid, enriched in the brain and retina, generates docosanoids in response to disruptions of cellular homeostasis. Docosanoids include neuroprotectin D1 (NPD1), which is decreased in the CA1 hippocampal area of patients with early-stage Alzheimer's disease (AD). We summarize here how NPD1 elicits neuroprotection by up-regulating c-REL, a nuclear factor (NF)-B subtype that, in turn, enhances expression of BIRC3 (baculoviral inhibitor of apoptosis repeat-containing protein 3) in the retina and in experimental stroke, leading to neuroprotection. Elucidating the mechanisms of action of docosanoids will contribute to managing diseases, including stroke, AD, age-related macular degeneration, traumatic brain injury, Parkinson's disease, and other neurodegenerations.

引用

页码：12390 / 12397

页数：8

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