Supplementary Material for: Expression of Angiogenic and Inflammatory Factors in Choroidal Neovascularisation-Derived Retinal Pigment Epithelium
收藏DataCite Commons2020-09-01 更新2024-07-25 收录
下载链接:
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Expression_of_Angiogenic_and_Inflammatory_Factors_in_Choroidal_Neovascularisation-Derived_Retinal_Pigment_Epithelium/5514037/1
下载链接
链接失效反馈官方服务:
资源简介:
<b><i>Purpose:</i></b> Anti-angiogenic treatment is well established in the management of exudative age-related macular degeneration (AMD), but not sufficient in all patients. The characterisation of factors driving this chronic disease could serve to identify additional treatment options. The purpose of this study was to assess gene expression patterns and distinct changes in cells derived from surgically extracted choroidal neovascularisation (CNV) membranes. <b><i>Materials and Methods:</i></b> The expression of >11,000 genes was analysed by means of a microarray in cells cultured from 2 late-stage CNV membranes compared to primary human retinal pigment epithelium (RPE) and ARPE-19 cells. A pathway analysis was performed to identify gene expression patterns associated with exudative AMD. <b><i>Results:</i></b> The analysis revealed significant alterations in gene sets associated with inflammatory processes in CNV-derived cells, involving the upregulation of pro-inflammatory factors IL6, C3, and C5, and downregulation of anti-inflammatory complement factor B and complement factor I. Factors associated with angiogenesis, such as VEGFA or ANGPT2, were not significantly regulated in the 2 RPE-derived cell lines. <b><i>Conclusion:</i></b> In late-stage CNV membrane-derived RPE, gene expression was shifted towards a pro-inflammatory state. Angiogenesis-associated factors were regulated differently in the 2 CNV-derived RPE membranes. While inflammation seems to be continuously stimulated by RPE associated with late exudative AMD, this appears not to be the case with regard to angioregulatory mechanisms.
提供机构:
Karger Publishers
创建时间:
2017-10-19



