May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
NAD(P)H Oxidase Regulates PPAR Expression in Models of Ischemic Retinopathy
Author Affiliations & Notes
  • M. A. Al-Shabrawey
    Oral Biology, School of Dentistry, Medical College of Georgia, Augusta, Georgia
  • T. L. Sanders
    Oral Biology, School of Dentistry, Medical College of Georgia, Augusta, Georgia
  • R. B. Caldwell
    Vascular Biology Center, Medical College of Georgia, Augusta, Georgia
  • Footnotes
    Commercial Relationships M.A. Al-Shabrawey, None; T.L. Sanders, None; R.B. Caldwell, None.
  • Footnotes
    Support Start up Funding from Medical College of Georgia
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4963. doi:
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      M. A. Al-Shabrawey, T. L. Sanders, R. B. Caldwell; NAD(P)H Oxidase Regulates PPAR Expression in Models of Ischemic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4963.

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

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Purpose:: We have recently demonstrated that reactive oxygen species derived from NAD(P)H oxidase are important for retinal neovascularization in a model of oxygen-induced retinopathy (OIR) as well as microvascular dysfunction during diabetic retinopathy as indicated by leukostasis and breakdown of the blood-retinal barrier. Peroxisome Proliferator-Activated Receptor γ (PPAR γ)is a member of a ligand-activated nuclear receptor superfamily and plays a critical role in angiogenesis and inflammation. The goal of this study was to investigate the role of PPAR γ in ischemic retinopathy and whether NAD(P)H oxidase regulates its expression in retina.

Methods:: Diabetes was induced in gp91phox +/+ and -/- mice with intraperitoneal injection of streptozotocin. One group of gp91+/+ mice was treated with apocynin (10mg/kg in drinking water). Expression of 12-Lipoxygnase (inflammatory mediator) and ICAM-1 (inflammatory marker) was investigated in retina of different groups with Western blotting and immunofluroscence. PPAR γ expression in retinal vessels was investigated in retinal sections from normal and 5 weeks diabetic mice using specific anti-PPAR γ antibody and isolectin B4 to label retinal vessels. PPAR γ expression was also investigated in retinal section from mice having OIR with or without apocynin treatment.

Results:: PPARγ is expressed in retinal vessels of normal animals. However, diabetes decreases PPARγ expression, and increases the expression of 12-lipoxygenase and ICAM-1. Inhibition of NAD(P)H oxidase by apocynin or deletion of gp91phox prevents diabetes-induced changes in the expression of PPARγ, 12-lipoxygenase and ICAM-1 in retina. Interestingly, PPARγ expression is also decreased in retina of mice with OIR and is restored by apocynin treatment.

Conclusions:: Ischemic retinopathy is associated with a decrease in PPAR γ and increases in inflammatory mediator and marker 12-lipoxygenase and ICAM-1. NAD(P)H oxidase might be a key mediator of these changes.

Keywords: diabetic retinopathy • oxidation/oxidative or free radical damage • inflammation 

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