June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Effect of Tissue Plasminogen Activator on Outflow Facility of Steroid Injected Mouse Eyes
Author Affiliations & Notes
  • Shaily Shah
    Cell Biology, SUNY Downstate Medical Center, Brooklyn, NY
    Mount Sinai School of Medicine, New York, NY
  • Sandeep Kumar
    Cell Biology, SUNY Downstate Medical Center, Brooklyn, NY
  • Terete Borras
    Ophthalmology, University of North Carolina School of Medicine, Chapel Hill, NC
  • Matthew Smith
    Ophthalmology, University of North Carolina School of Medicine, Chapel Hill, NC
  • John Danias
    Cell Biology, SUNY Downstate Medical Center, Brooklyn, NY
    Ophthalmology, SUNY Downstate Medical Center and SUNY Eye Institute, Brooklyn, NY
  • Footnotes
    Commercial Relationships Shaily Shah, None; Sandeep Kumar, None; Terete Borras, None; Matthew Smith, None; John Danias, Bausch and Lomb (C), N/A (P)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 788. doi:
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    • Get Citation

      Shaily Shah, Sandeep Kumar, Terete Borras, Matthew Smith, John Danias; Effect of Tissue Plasminogen Activator on Outflow Facility of Steroid Injected Mouse Eyes. Invest. Ophthalmol. Vis. Sci. 2013;54(15):788.

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

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Abstract

Purpose: To determine whether over-expression of the tissue plasminogen activator (PLAT) gene can increase outflow facility in a mouse model of steroid-induced glaucoma

Methods: Adenoviral vectors carrying cDNA of the sheep PLAT gene and a fluorescent reporter gene (mCherry) (AdPLAT) or with no transgene (AdNull) were created. Transgene expression was driven by the CMV promoter. 3 groups of C57/B6 mice received either: 1. 20µl of triamcinolone acetonide (TA) suspension (40mg/ml) subconjunctivally bilaterally followed immediately by unilateral intracameral injection with 2µl AdPLAT (3-4x1012 VG/ml) 2. 20µl TA subconjunctivally bilaterally followed one week later by unilateral intracameral injection with 2µl AdPLAT 3. 20µl TA subconjunctivally bilaterally followed immediately by bilateral injection with 2µl AdNull IOP was measured preterminally. Outflow facility was determined using simultaneous pressure and flow measurements. After outflow facility measurement, all AdPLAT injected eyes were dissected and viewed under a fluorescent microscope to inspect for mCherry expression in the trabecular meshwork (TM). Eyes that showed mCherry expression were analyzed as a separate group from eyes that showed minimal mCherry expression.

Results: IOP was not significantly different between all eye groups (p>0.05) after either one or two weeks of treatment with TA. Eyes subjected to one week of TA treatment that showed mCherry/PLAT expression had 63%, 54%, and 31% higher outflow facility than AdPLAT treated eyes with minimal mCherry/PLAT expression, contralateral control eyes, and AdNull treated eyes respectively (ANOVA, p<0.05). Eyes subjected to two weeks of TA treatment that showed mCherry/PLAT expression had 86% and 58% higher outflow facility than AdPLAT treated eyes with minimal mCherry/PLAT expression and contralateral control eyes respectively (ANOVA, p<0.05).

Conclusions: Treatment with AdPLAT can both prevent and reverse the decrease in outflow facility caused by steroid treatment in mice.

Keywords: 633 outflow: trabecular meshwork • 421 anterior segment • 568 intraocular pressure  
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