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Christina Korb, Sabine Beck, Katrin Lorenz, Alireza Mirshahi, Bernhard Stoffelns, Norbert Pfeiffer, Franz Grus; Serum protein analysis of patients with different vitreoretinal diseases by means of antibody microarrays. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3332.
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© ARVO (1962-2015); The Authors (2016-present)
To develop a comparative proteome analysis of human serum samples in patients with various vitreoretinal diseases to provide insights into factors and mechanisms responsible for these diseases.
Serum samples were collected from 63 patients with macular pucker (n=19), idiopathic macular hole (n=16), proliferative diabetic retinopathy (DR, n=10), rhegmatogenous (n=6) or tractional (n=9) retinal detachment and neovascular age-related macular degeneration (AMD, n=3). As control group, serum samples from 27 healthy subjects were used. Protein expression levels were estimated using customized antibody microarrays. The 29 spotted antibodies represented families of proteins known to be involved in a variety of important biological pathways, including heat shock proteins (HSPs), proteins of the complement pathway and cytokines. Emitted fluorescence signals were digitized and spot intensities were compared to estimate changes in protein expression.
Complex patterns of proteins could be detected in all clinical groups. Furthermore, differences in mean protein intensity could be detected in all diseases in comparison to the control cohort. Mean intensities of some proteins, e.g. Interleukin 2, HSP 27, and Protein S100A8 were lower in serum in all clinical groups compared controls. Some of the detected protein levels were about 3 fold higher in only some clinical groups , for example PEDF: > 3.6 change in AMD or Il-1-beta: > 2.8 in DR. With respect to the control subjects with no ocular disease, protein abundance of complement protein C9, HSP 90 and HSP 70 was lower in serum especially in the group of patients with neovascular age-related macular degeneration (protein expression in patients compared to controls is decreased about 50%).
Our study provides a proteomic analysis of the serum proteome and reveals protein alterations in the included clinical groups compared to the group of healthy subjects. Each vitreoretinal disease altered a unique set of proteins. These potential biomarkers could lead to new insights in underlying pathomechanisms of the analyzed diseases.
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