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Astrocyte activation and reactive gliosis.星形胶质细胞激活与反应性胶质增生。
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Glial nitric oxide and ischemia.神经胶质细胞一氧化氮与缺血
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Role of MAPK/ERK1/2 in the glucose deprivation-induced death in immunostimulated astroglia.丝裂原活化蛋白激酶/细胞外信号调节激酶1/2(MAPK/ERK1/2)在免疫刺激的星形胶质细胞中葡萄糖剥夺诱导的死亡中的作用
Neurosci Lett. 2005 Mar 16;376(3):171-6. doi: 10.1016/j.neulet.2004.11.077. Epub 2004 Dec 19.
7
Knock your SOCS off!把你的细胞因子信号转导抑制蛋白敲除掉!
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8
Regulation of inducible nitric oxide synthase in proinflammatory cytokine-stimulated human primary astrocytes.促炎细胞因子刺激的人原代星形胶质细胞中诱导型一氧化氮合酶的调控
Free Radic Biol Med. 2005 Mar 1;38(5):655-64. doi: 10.1016/j.freeradbiomed.2004.11.021.
9
Dual role of cAMP in iNOS expression in glial cells and macrophages is mediated by differential regulation of p38-MAPK/ATF-2 activation and iNOS stability.环磷酸腺苷(cAMP)在神经胶质细胞和巨噬细胞诱导型一氧化氮合酶(iNOS)表达中的双重作用是由p38丝裂原活化蛋白激酶(p38-MAPK)/活化转录因子2(ATF-2)激活的差异调节和iNOS稳定性介导的。
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The 15-deoxy-delta12,14-prostaglandin J2 inhibits the inflammatory response in primary rat astrocytes via down-regulating multiple steps in phosphatidylinositol 3-kinase-Akt-NF-kappaB-p300 pathway independent of peroxisome proliferator-activated receptor gamma.15-脱氧-Δ12,14-前列腺素J2通过下调磷脂酰肌醇3-激酶-Akt-NF-κB-p300途径中的多个步骤来抑制原代大鼠星形胶质细胞中的炎症反应,该过程独立于过氧化物酶体增殖物激活受体γ。
J Immunol. 2004 Oct 15;173(8):5196-208. doi: 10.4049/jimmunol.173.8.5196.

星形胶质细胞中一氧化氮合酶诱导的信号

Signals for the induction of nitric oxide synthase in astrocytes.

作者信息

Saha Ramendra N, Pahan Kalipada

机构信息

Section of Neuroscience, Department of Oral Biology, University of Nebraska Medical Center College of Dentistry, 40th and Holdrege, Lincoln, NE 68583, United States.

出版信息

Neurochem Int. 2006 Jul;49(2):154-63. doi: 10.1016/j.neuint.2006.04.007. Epub 2006 Jun 5.

DOI:10.1016/j.neuint.2006.04.007
PMID:16740341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1963413/
Abstract

Nitric oxide (NO), being a double-edged sword depending on its concentration in the microenvironment, is involved in both physiological and pathological processes of many organ systems including brain and spinal cord. It is now well-documented that once inducible nitric oxide synthase (iNOS) is expressed in CNS in a signal-dependent fashion, NO in excess of physiological thresholds is produced and this excess NO then plays a role in the pathogenesis of stroke, demyelination and other neurodegenerative diseases. Therefore, a keen interest has been generated in recent years in comprehending the regulation of this enzyme in brain cells. The present review summarizes our current understanding of signaling mechanisms leading to transcription of the iNOS gene in activated astrocytes. We attempt this comprehension with a hope to identify potential targets to intervene NO-mediated CNS disorders.

摘要

一氧化氮(NO)根据其在微环境中的浓度扮演着双刃剑的角色,参与包括脑和脊髓在内的许多器官系统的生理和病理过程。现在有充分的文献记载,一旦诱导型一氧化氮合酶(iNOS)以信号依赖的方式在中枢神经系统中表达,就会产生超过生理阈值的NO,而这种过量的NO随后在中风、脱髓鞘和其他神经退行性疾病的发病机制中发挥作用。因此,近年来人们对理解这种酶在脑细胞中的调节产生了浓厚的兴趣。本综述总结了我们目前对激活的星形胶质细胞中导致iNOS基因转录的信号机制的理解。我们尝试进行这种理解,希望能确定干预NO介导的中枢神经系统疾病的潜在靶点。