NOD‐like receptor protein 3 (NLRP3) is associated with age‐related macular degeneration (AMD). Retinal pigment epithelial (RPE) cells serve as the immune defense of macula, and their dysfunction causes clinically relevant changes in AMD. In the present study, oxidized low‐density lipoprotein (ox‐LDL) activated the NLRP3 inflammasome in human RPE cell line ARPE‐19. Our data showed that the expression of NLRP3, interleukin‐1β (IL‐1β), and caspase‐1 and the release of IL‐1β in ARPE‐19 cells were substantially increased by ox‐LDL, whereas the addition of NLRP3 inhibitor INF39 dose‐dependently reversed the effect of ox‐LDL. Overexpression of tripartite motif‐containing protein 31 (TRIM31) also suppressed the effect of ox‐LDL in ARPE‐19 cells. TRIM31 knockdown had similar effects with ox‐LDL but INF39 could block the effect of TRIM31 knockdown. Moreover, TRIM31 could interact with NLRP3 in ARPE‐19 cells. Overexpression of TRIM31 increased NLRP3 ubiquitination. In conclusion, the results propose that TRIM31 could enhance NLRP3 ubiquitination, therefore inhibiting NLRP3 inflammasome and pyroptosis in human RPE cells.

中文翻译：

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TRIM31通过泛素化NLRP3抑制NLRP3炎症小体和视网膜色素上皮细胞的热凋亡。

NOD样受体蛋白3（NLRP3）与年龄相关性黄斑变性（AMD）相关。视网膜色素上皮（RPE）细胞可作为黄斑的免疫防御系统，其功能障碍会引起AMD的临床相关变化。在本研究中，氧化的低密度脂蛋白（ox-LDL）激活了人RPE细胞ARPE-19中的NLRP3炎性小体。我们的数据显示ox-LDL大大增加了ARPE-19细胞中NLRP3，白介素-1β（IL-1β）和caspase-1的表达以及IL-1β的释放，而添加NLRP3抑制剂INF39剂量相应地逆转了ox-LDL的作用。包含三重基序基序的蛋白31（TRIM31）的过表达也抑制了ARPE-19细胞中ox-LDL的作用。TRIM31敲除与ox-LDL具有相似的作用，但INF39可以阻断TRIM31敲除的作用。此外，TRIM31可以与ARPE-19细胞中的NLRP3相互作用。TRIM31的过表达增加了NLRP3泛素化。总之，结果表明，TRIM31可以增强NLRP3泛素化，从而抑制人RPE细胞中的NLRP3炎性体和发烧。