Tumor necrosis factor-alpha mediated signaling in neuronal homeostasis and dysfunction

被引:340
作者
Park, Keigan M. [1 ,4 ]
Bowers, William J. [1 ,2 ,3 ,4 ]
机构
[1] Univ Rochester, Ctr Neural Dev & Dis, Med Ctr, Sch Med & Dent, Rochester, NY 14642 USA
[2] Univ Rochester, Med Ctr, Dept Neurol, Rochester, NY 14642 USA
[3] Univ Rochester, Med Ctr, Dept Microbiol & Immunol, Rochester, NY 14642 USA
[4] Univ Rochester, Med Ctr, Dept Physiol & Pharmacol, Rochester, NY 14642 USA
关键词
TNF-alpha; Neuroinflammation; Alzheimer's; Parkinson's; Synaptic plasticity; Ionic homeostasis; NF-KAPPA-B; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; LONG-TERM POTENTIATION; ALZHEIMERS-DISEASE; TNF-ALPHA; PARKINSONS-DISEASE; CELL-DEATH; MICROGLIAL ACTIVATION; TRANSGENIC MICE;
D O I
10.1016/j.cellsig.2010.01.010
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Tumor necrosis factor-alpha (TNF-alpha) is a potent pro-inflammatory molecule, which upon engagement with its cognate receptors on target cells, triggers downstream signaling cascades that control a number of cellular processes related to cell viability, gene expression, ion homeostasis, and synaptic integrity. In the central nervous system (CNS), TNF-alpha is produced by brain-resident astrocytes, microglia, and neurons in response to numerous intrinsic and extrinsic stimuli. This review will summarize the key events that lead to TNF-alpha elaboration in the CNS, and the effects that these inflammatory signals impart on neuronal signaling in the context of homeostasis and neuropathology. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:977 / 983
页数:7
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