Department of Cellular and Molecular Medicine, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
The HNPCC Register, Clinical Research Department, Copenhagen University Hospital, Hvidovre, Denmark.
Sci Rep. 2021 Apr 15;11(1):8226. doi: 10.1038/s41598-021-87337-1.
Age-related macular degeneration (AMD) is a highly prevalent degenerative disease and a leading cause of vision loss worldwide. Evidence for an inflammatory component in the development of AMD exists, yet the exact mechanisms remain unclear. Bisretinoid N-retinylidene-N-retinylethanolamine (A2E) in retinal pigmental epithelial (RPE) cells, and in extracellular deposits constitutes a hallmark of AMD, but its role in the pathology of AMD is elusive. Here, we tested the hypothesis that A2E is responsible for the heightened inflammatory activity in AMD. To this end, we measured ex vivo mRNA expression of the cytokines TNF-α, IL-6, and IL-10 in whole blood samples after stimulation with A2E in a clinical sample of 27 patients with neovascular AMD and 24 patients with geographic atrophy secondary to AMD. Patients' spouses (n = 30) were included as non-affected controls. After stimulation with A2E, no statistical differences were found in the median expression level of TNF-α, IL-6, IL-10 between the control group, and the neovascular AMD and the geographic atrophy group. Our findings do not support evidence for the hypothesis, that A2E per se contributes to heightened inflammatory activity in AMD.
年龄相关性黄斑变性（AMD）是一种高度普遍的退行性疾病，也是全球视力丧失的主要原因。存在 AMD 发展中炎症成分的证据，但确切机制仍不清楚。视网膜色素上皮（RPE）细胞中的双视黄醇 N-视黄醛基-N-视黄基乙胺（A2E）和细胞外沉积物是 AMD 的标志，但它在 AMD 病理学中的作用尚不清楚。在这里，我们检验了 A2E 是否负责 AMD 中炎症活性增加的假设。为此，我们在 27 名新生血管性 AMD 患者和 24 名继发于 AMD 的地理萎缩患者的临床样本中，测量了全血样本在 A2E 刺激后细胞因子 TNF-α、IL-6 和 IL-10 的外显子 mRNA 表达。患者的配偶（n=30）被纳入无影响的对照组。在用 A2E 刺激后，对照组、新生血管性 AMD 组和地理萎缩组之间 TNF-α、IL-6、IL-10 的中位表达水平没有统计学差异。我们的研究结果不支持 A2E 本身导致 AMD 炎症活性增加的假设。
