April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Pathophysiology of Outer Blood-Retina Barrier Breakdown
Author Affiliations & Notes
  • Y.-Z. Le
    Medicine, Cell Biology, and Harold Hamm Oklahoma Diabetes Center,
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Dean A. McGee Eye Institute, Oklahoma City, Oklahoma
  • J. Wang
    Medicine and Harold Hamm Oklahoma Diabetes Center,
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Ophthalmology, Xiangya Hospital, Central South University, Changsha, China
  • H. Xu
    Medicine and Harold Hamm Oklahoma Diabetes Center,
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Ophthalmology, Xiangya Hospital, Central South University, Changsha, China
  • Footnotes
    Commercial Relationships  Y.-Z. Le, None; J. Wang, None; H. Xu, None.
  • Footnotes
    Support  NIH grants P20RR17703, P20RR024215, P30EY12190, ADA grants 1-06-RA-76, 1-10-BS-94, AHAF grant M2008-059, FFB grant BR-CMM-0808-0453-UOK, OCAST grant HR09-058
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 498. doi:
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    • Get Citation

      Y.-Z. Le, J. Wang, H. Xu; Pathophysiology of Outer Blood-Retina Barrier Breakdown. Invest. Ophthalmol. Vis. Sci. 2010;51(13):498.

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

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Abstract

Purpose: : Although outer blood-retina (BRB) barrier is responsible for approximately 80% of blood circulation in the retina, the pathophysiology of outer BRB is not well-studied. To determine the significance of outer BRB breakdown in retinal vascular diseases, we investigated outer BRB-specific leakage in mice with altered RPE barrier in ischemia and uveitis models.

Methods: : Mice with altered outer BRB were generated by disrupting vascular endothelial growth factor (VEGF) or VEGF-receptor 2 (R2) in the RPE. Ischemia was induced with an oxygen-induced retinopathy (OIR) and uveitis was generated with endotoxin-induced uveitis (EIU). The alteration of outer BRB was assessed by measuring tight-junction protein occludin in the RPE with Western blot and immunohistochemistry. The outer BRB-specific leakage of macromolecules were visualized and measured by a fluorescent microscopic assay.

Results: : For the first time, we were able to visualize and measure outer BRB-specific leakage in ischemic mice. Outer BRB-specific breakpoints and macromolecule leakage were significantly reduced in the OIR-treated conditional VEGF or VEGF-R2 KO mice. EIU-treated conditional VEGF KO mice demonstrated a significant reduction in the size of retinal detachments and the amount of outer BRB-specific leakage. These pathological changes were associated with an attenuation of occludin depletion in the conditional VEGF or VEGF-R2 KO mice.

Conclusions: : Our newly established fluorescent microscopic assay permits the visualization and measurement of outer BRB breakdown in ischemic mice for the first time. Our results suggest that the breakdown of outer BRB contributes significantly to overall blood-content leakage under ischemic condition and exudative retinal detachment under uveitic condition, through an autocrine VEGF signaling mechanism. Therefore, our study may have significant implications to the mechanism, diagnosis, and therapeutics of retinopathy of prematurity, uveitis, and macular edema.

Keywords: retinopathy of prematurity • uveitis-clinical/animal model • edema 
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