May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Analysis of TGF–ß1 Activation by Inflammatory Cytokine TNF–
Author Affiliations & Notes
  • J.M. Gonzalez
    University of Oklahoma Health Sciences Center, Oklahoma City, OK
    Cell Biology,
  • J.D. Ash
    University of Oklahoma Health Sciences Center, Oklahoma City, OK
    Ophthalmology,
  • Footnotes
    Commercial Relationships  J.M. Gonzalez, None; J.D. Ash, None.
  • Footnotes
    Support  NIH Grant EY14206, EY012190, RR017703, and RPB
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1724. doi:
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      J.M. Gonzalez, J.D. Ash; Analysis of TGF–ß1 Activation by Inflammatory Cytokine TNF– . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1724.

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

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Abstract

Purpose: : We have previously shown that increased expression of activated TGF–ß1 causes similar ocular complications found in diabetic patients, including abnormal retinal blood vessels due to disrupted recruitment of retinal pericytes, lens cataracts, and corneal opacities. The long–term goal of this study is to determine if inflammatory cytokines cause the activation of transforming growth factor beta 1 (TGF–b1) that is observed in diabetic patients. The purpose of this study is to determine whether or not cytokines such as tumor necrosis factor alpha (TNF–α) can cause TGF–ß1 activation in vivo.

Methods: : Recombinant TNF–α was injected into the vitreous of BalbC mice. Two days after injection, TGF–ß1 was measured by ELISA specific for activated TGF–ß1. Vascular permeability was also used to monitor the integrity of the blood retinal barrier.

Results: : Intravitreal injections of TNF–α led to activation of TGF–ß1 when compared to PBS injected controls.

Conclusions: : Our previous studies have shown that elevated expression of activated TGF–ß1 causes disruptions in the retinal vasculature including failure of pericyte recruitment. Data from this study suggest that inflammation induced by diabetes may result in activation of endogenous TGF–ß1.

Keywords: diabetic retinopathy • cytokines/chemokines • inflammation 
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