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Matthew S J Katz, Alexandre F Gauthier, Bert M Glaser; Vitreous Proteomics Demonstrates That TGFβ and TGFβR Parallel Severity of Diabetic Macular Edema. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4714.
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© ARVO (1962-2015); The Authors (2016-present)
The biochemical pathways in the development of Diabetic Macular Edema (DME) are poorly understood. Increasing evidence suggests that inflammation may play a role. Transforming Growth Factor β (TGFβ) is a cytokine involved in inflammation and angiogenesis. Therefore, we examined the correlation of vitreous levels of TGFβ and its receptor, Transforming Growth Factor β Receptor (TGFβR) with DME.
In-office vitreous aspirates (50-100 μL) were obtained from 20 eyes of 16 patients treated for DME with Anti-VEGF agents during the period between 11/26/08 and 10/22/09 during an IRB approved study. Each vitreous sample was acquired immediately prior to intra-vitreal injection at initiation of treatment. All vitreous samples were investigated utilizing Reverse Phase Protein Microarray (RPPM) technology. Spectral Domain-OCT was conducted preceding treatment and maximum macular thickness (MMT) was determined. Correlation was measured using Pearson’s Analysis.
20 samples obtained from 20 eyes of 16 subjects were studied. Correlation coefficients between TGFβ and MMT, CMT, and TV were -0.0311, -0.0366, and -0.1123 respectively. TGFβR was found to have correlation coefficients of -0.1428, -0.119, and -0.0297 with MMT, CMT, and TV respectively.
In-office vitreous sampling reveals an inverse relationship between TGFβ and TGFβR levels with the severity of DME. This suggests that the TGF-beta pathway may be involved in angiogenesis and inflammation in DME and might deserve further investigation.
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