June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Elevated TGFβ1 concentration in the plasma of glaucoma patients
Author Affiliations & Notes
  • John Kuchtey
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
  • L. Goodwin Burgess
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
  • Megan Parks
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
  • Jessica Kunkel
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
  • Milam Brantley
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
  • Rachel Kuchtey
    Vanderbilt Eye Institute, Vanderbilt University, Nashville, TN
  • Footnotes
    Commercial Relationships John Kuchtey, None; L. Goodwin Burgess, None; Megan Parks, None; Jessica Kunkel, None; Milam Brantley, None; Rachel Kuchtey, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 1597. doi:
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    • Get Citation

      John Kuchtey, L. Goodwin Burgess, Megan Parks, Jessica Kunkel, Milam Brantley, Rachel Kuchtey; Elevated TGFβ1 concentration in the plasma of glaucoma patients. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1597.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Previously, we formed the hypothesis that microfibril defects may contribute to glaucoma pathogenesis, based on our identification of the microfibril-associated gene, ADAMTS10, as the disease gene in a colony of dogs with inherited primary open angle glaucoma (POAG). Since microfibrils are a major reservoir for TGFβ, and because other diseases caused by defective microfibrils are associated with elevated plasma TGFβ, a corollary to the microfibril hypothesis is that glaucoma patients may have a systemic elevation of TGFβ. The purpose of this study was to test the hypothesis that patients with POAG have elevated plasma concentrations of TGFβ.

Methods: Blood samples from POAG patients and controls were collected in lithium heparin tubes, centrifuged at 4 oC for 10 minutes at 1,500 x g and plasma aliquoted and stored at -80 oC. Concentrations of total TGFβ1 and total TGFβ2 were determined by ELISA assay of acid-activated plasma samples from POAG patients and controls matched for age, sex and ancestry.

Results: In an initial set of 55 POAG patients and 55 controls, total TGFβ1 was higher in the plasma of POAG patients compared to controls (median concentrations 3.12 vs. 2.54 ng/ml, respectively, p<0.05 by Mann-Whitney Test). A wider distribution of total TGFβ1 concentrations was observed for the POAG group, with a subset of patients having concentrations >2SD above the mean of controls. Plasma total TGFβ2 concentrations were below limits of detection.

Conclusions: Total TGFβ1 is higher in the plasma of POAG patients as compared to controls, with some patients having pronounced elevation. This finding is consistent with our hypothesis that defective microfibrils contribute to glaucoma pathogenesis and suggest a mechanism to explain elevated TGFβ in the aqueous humor of glaucoma patients. Elevated plasma TGFβ1 may be used as a biomarker for glaucoma associated with defective microfibrils.

Keywords: 533 gene/expression • 660 proteins encoded by disease genes • 427 aqueous  
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