June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Vitreous Proteomics Demonstrates That TGFβ and TGFβR Parallel Severity of Diabetic Macular Edema
Author Affiliations & Notes
  • Matthew S J Katz
    National Retina Institute, Towson, MD
  • Alexandre F Gauthier
    National Retina Institute, Towson, MD
  • Bert M Glaser
    National Retina Institute, Towson, MD
  • Footnotes
    Commercial Relationships Matthew Katz, None; Alexandre Gauthier, None; Bert Glaser, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4714. doi:
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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)

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Purpose: 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.

Methods: 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.

Results: 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.

Conclusions: 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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