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Sandeep Kumar, Shaily Shah, Emily Deutsch, Hai Tang, John Danias; Effect of anecortave acetate (AA) on outflow facility in a mouse model of steroid-induced glaucoma. Invest. Ophthalmol. Vis. Sci. 2013;54(15):782.
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To determine the effect of AA on the outflow facility in a mouse model of steroid-induced glaucoma.
Four groups of C57/B6 mice received either i. 20µl of Triamcinolone acetonide (TA) (40mg/ml) subconjunctivally bilaterally followed by AA (75mg/ml, Alcon) two weeks later, ii. TA for 3 weeks, iii. AA for 1 week iv. No intervention. IOP was measured preteminally. Outflow facility was determined using simultaneous pressure and flow measurements. Myocilin expression was investigated in a subset of eyes using quantitative PCR.
Eyes receiving TA had significantly decreased outflow facility compared to naïve control eyes (p<0.05, t-test). Outflow facility was significantly higher (p<0.05) in eyes receiving both TA and AA, and eyes receiving AA alone compared to eyes receiving TA alone but .not significantly different from that of naïve control eyes. Eyes receiving AA either alone or together with TA had significantly lower (p<0.001, ANOVA) relative MYOC expression compared to either TA injected or naïve control eyes. IOP was not significantly different among groups of eyes (p>0.05).
Treatment with AA can reverse the decrease in outflow facility caused by steroid treatment in mice. Myocilin expression is not affected by TA treatment in mice but is affected by AA.
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