May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Caveolin 1 Is Essential to Maintain Blood Vessel Integrity in the Mouse Retina
Author Affiliations & Notes
  • J.D. Ash
    Ophthalmology, Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
    Dean A. McGee Eye Institute, Oklahoma City, OK
  • R.S. Charrad
    Ophthalmology, Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
    Dean A. McGee Eye Institute, Oklahoma City, OK
  • R. Archer
    Ophthalmology, Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
    Dean A. McGee Eye Institute, Oklahoma City, OK
  • M.E. Elliott
    Ophthalmology, Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
    Dean A. McGee Eye Institute, Oklahoma City, OK
  • Footnotes
    Commercial Relationships  J.D. Ash, None; R.S. Charrad, None; R. Archer, None; M.E. Elliott, None.
  • Footnotes
    Support  NIH grants P20 RR017703, EY14206–03, and P30 EY012190. OCAST HR02140RS. Research to Prevent Blindnes
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4709. doi:
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    • Get Citation

      J.D. Ash, R.S. Charrad, R. Archer, M.E. Elliott; Caveolin 1 Is Essential to Maintain Blood Vessel Integrity in the Mouse Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4709.

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

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Abstract

Abstract: : Purpose: Caveolin 1 (Cav–1) is an important membrane organizing protein that binds and regulates the function of essential angiogenic signaling molecules in vascular endothelial cells. Cav–1 is a negative regulation of VEGFR2, and eNOS, and is likely to play an important role in regulating vascular stability and angiogenesis. The purpose of this study was to determine the role of Cav–1 in regulating retinal vascular development and vascular stability in the oxygen induce retinopathy model. Methods: Retinas were dissected from mice reared in normal oxygen conditions, and from mice exposed to elevated oxygen. The retinal vasculature was stained using Griffionia simplicifilia lectin (isotype B4), and the retinas were flat mounted fro microscopy. For the oxygen exposure we placed Cav–1 knockout mice in 75% oxygen from postnatal day 7 to 13. Mice were then returned to room air until postnatal day 17. Neovascularization was quantified by counting preretinal vascular tufts on confocal images. Results: In room air control mice we observed that retinal vessels were significantly dilated compared to control mice. In the oxygen induced retinopathy model we observed similar levels of neovascularization in knockout and control mice. However, 100% of knockout mice had severe intra–retinal hemorrhaging while none of the control mice did. Conclusions: Cav–1 is an important regulator of vascular function and stability in the retina. The absence of Cav–1 results in a phenotype that is consistent with deregulated eNOS, and overstimulation of VEGFRs. The results suggest that Cav–1 may be an important target to regulate angiogenic signaling molecules.

Keywords: diabetic retinopathy • neovascularization • transgenics/knock-outs 
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