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RPE 中泛素-蛋白酶体途径的损伤改变了炎症相关基因的表达。

Impairment of the ubiquitin-proteasome pathway in RPE alters the expression of inflammation related genes.

机构信息

Laboratory for Nutrition and Vision Research, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, USA,

出版信息

Adv Exp Med Biol. 2014;801:237-50. doi: 10.1007/978-1-4614-3209-8_31.

DOI:10.1007/978-1-4614-3209-8_31
PMID:24664704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4828937/
Abstract

The ubiquitin-proteasome pathway (UPP) plays an important role in regulating gene expression. Retinal pigment epithelial cells (RPE) are a major source of ocular inflammatory cytokines. In this work we determined the relationship between impairment of the UPP and expression of inflammation-related factors. The UPP could be impaired by oxidative stress or chemical inhibition. Impairment of the UPP in RPE increased the expression of several inflammatory cytokines, such as IL-6 and IL-8. However, the expression of monocyte chemoattractant protein-1 (MCP-1) and complement factor H (CFH) and was reduced upon impairment of the UPP. These data suggest that impairment of the UPP in RPE may be one of the causes of retinal inflammation and abnormal functions of monocyte and the complement system during the pathogenesis of age-related macular degeneration.

摘要

泛素-蛋白酶体途径(UPP)在调节基因表达中起着重要作用。视网膜色素上皮细胞(RPE)是眼部炎症细胞因子的主要来源。在这项工作中,我们确定了 UPP 损伤与炎症相关因子表达之间的关系。UPP 可被氧化应激或化学抑制损伤。RPE 中 UPP 的损伤增加了几种炎症细胞因子的表达,如 IL-6 和 IL-8。然而,单核细胞趋化蛋白-1(MCP-1)和补体因子 H(CFH)的表达在 UPP 损伤时减少。这些数据表明,RPE 中 UPP 的损伤可能是年龄相关性黄斑变性发病过程中视网膜炎症以及单核细胞和补体系统异常功能的原因之一。

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本文引用的文献

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Mol Aspects Med. 2012 Aug;33(4):446-66. doi: 10.1016/j.mam.2012.04.001. Epub 2012 Apr 10.
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Ubiquitin-proteasome pathway and cellular responses to oxidative stress.泛素-蛋白酶体通路与细胞对氧化应激的反应。
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7-ketocholesterol-induced inflammation: involvement of multiple kinase signaling pathways via NFκB but independently of reactive oxygen species formation.7-酮胆固醇诱导的炎症:通过核因子κB(NFκB)涉及多种激酶信号通路,但与活性氧生成无关。
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Targeting the vicious inflammation-oxidative stress cycle for the management of heart failure.针对心力衰竭的恶性循环——炎症-氧化应激进行治疗。
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Prog Retin Eye Res. 2010 Mar;29(2):95-112. doi: 10.1016/j.preteyeres.2009.11.003. Epub 2009 Dec 2.
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Sustained oxidative stress inhibits NF-kappaB activation partially via inactivating the proteasome.持续的氧化应激通过使蛋白酶体失活部分抑制核因子κB的激活。
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