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

Impairment of the ubiquitin-proteasome pathway in RPE alters the expression of inflammation related genes.
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DOI:
10.1007/978-1-4614-3209-8_31
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发表时间:
2014
影响因子:
--
通讯作者:
Shang F
Shang F
中科院分区:
医学4区
文献类型:
--
作者:
Liu Z;Qin T;Zhou J;Taylor A;Sparrow JR;Shang F

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泛素-蛋白酶体途径(UPP)在调控基因表达中起着重要作用。视网膜色素上皮细胞(RPE)是眼部炎性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可因氧化应激或化学抑制而受损。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损伤后降低。这些数据提示,在老年性黄斑变性发病过程中,RPE中UPP的损伤可能是视网膜炎症以及单核细胞和补体系统功能异常的原因之一。
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.