May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Statin Treatment Is Protective for Oxygen–Induced Retinal Microvascular Injury
Author Affiliations & Notes
  • M. Istanboli
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • M. Al–Shabrawey
    Vascular Biology Center,
    Medical College of Georgia, Augusta, GA
  • M.A. Behzadian
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • T. Franklin
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • T. Lemtalsi
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • D.H. Platt
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • A.B. El–Remessy
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • R.B. Caldwell
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • M. Bartoli
    Internal Medicine,
    Medical College of Georgia, Augusta, GA
  • Footnotes
    Commercial Relationships  M. Istanboli, None; M. Al–Shabrawey, None; M.A. Behzadian, None; T. Franklin, None; T. Lemtalsi, None; D.H. Platt, None; A.B. El–Remessy, None; R.B. Caldwell, None; M. Bartoli, None.
  • Footnotes
    Support  Fight For Sight, AHA, EY011766,EY004618
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 466. doi:
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      M. Istanboli, M. Al–Shabrawey, M.A. Behzadian, T. Franklin, T. Lemtalsi, D.H. Platt, A.B. El–Remessy, R.B. Caldwell, M. Bartoli; Statin Treatment Is Protective for Oxygen–Induced Retinal Microvascular Injury . Invest. Ophthalmol. Vis. Sci. 2005;46(13):466.

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

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Abstract

Abstract: : Purpose: The present study is aimed at determining the effect of statin treatment in preventing oxygen–induced retinal vascular injury. Oxygen–induced vascular injury is a major cause of retinopathy and blindness in infants. Recent studies have shown that inhibitors of HMG–CoA reductase (statins) exert remarkable vasoprotective effects independently of their lipid lowering properties. Statins exert their protective effects also on the retinal microvasculature, as has been shown in a number of disease conditions including diabetic retinopathy and age–related macular degeneration. Methods: Experiments were done in the mouse model of oxygen–induced retinopathy (OIR) in which neonatal mice are maintained in 75% oxygen for 5 days (vaso–obliteration period) followed by 5days in normoxia (relative ischemia period). Mice were treated with fluvastatin (10mg/Kg/day) or with saline during the time of exposure to high oxygen levels. Vascular obliteration was then evaluated by morphometric analysis using retinal flatmounts labeled with texas–red isolectin B4. Western blotting analysis was used to determine the retinal levels of vascular endothelial growth factor (VEGF). The malondialdheyde (MDA) technique was used to determine lipid peroxidation levels in the retinal extracts, as indicator of oxidative stress. Results: The morphometric analysis of retinal flatmounts showed that fluvastatin treatment significantly (p<0.05, n=14) reduced capillary dropout in the OIR retinas. Furthermore, the fluvastatin treatment significantly (p<0.01, n=14) prevented lipid peroxidation induced by the high oxygen treatment. Finally, retinal levels of the angiogenic cytokine vascular endothelial growth factor (VEGF) were decreased by the exposure to high oxygen levels and the statin treatment prevented this effect. Conclusions: Our results indicate that statin treatment effectively protects the developing retinal microvasculature during exposure to hyperoxic conditions and prevent oxygen–induced vascular drop–out. This effect is associated with decreased levels of oxidative stress and with preservation of normal expression levels of the endothelial cell survival factor VEGF.

Keywords: ischemia • retinopathy of prematurity • cell death/apoptosis 
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