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P.D. Jani, N. Singh, A. Behzadian, R. Caldwell, T. Franklin, B. Ambati; Silver Nitrate Injury to Mouse Cornea Induces MMPs and Decreases sFlt Protein, but Increases sFlt Genetic Expression . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1648.
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The molecular basis of the cornea’s avascularity and response to injury remain to be elucidated. Silver nitrate injury typically induces a brief angiogenic response adjacent to the site of corneal injury. In this study, we sought to determine the effects of silver nitrate cauterization on MMP–2, MMP–9 (pro–angiogenic matrix metalloproteinases) and sFlt (soluble VEGF receptor–1, an anti–angiogenic factor) levels in the mouse cornea.
Juxtalimbal burns are administered to mouse corneas using shaved silver nitrate sticks. Corneas are sectioned into vascular and non–vascular halves 7 days after initial burns are made. MMP–2 and MMP–9 expression in vascular, non–vascular, and control (uninjured) corneas are assessed using gelatin zymography. sFlt genetic expression is assessed using RT–PCR. sFlt protein levels are assessed by Western blot.
MMP–9 and activated MMP–2 levels are increased in vascularized corneal sections by 130% and 310%, respectively. Inactive MMP–2 levels are slightly decreased, by approximately 15%. sFlt protein levels are qualitatively reduced in neovascularized corneas. Genetic expression of sFlt is somewhat elevated in vascular samples tested by sFlt RT–PCR.
We found that silver nitrate injury elicits a complex interplay of biochemical and genetic responses in the mouse cornea. Activated MMP–2 and MMP–9 expression increase while sFlt levels decrease in corneal sections adjacent to the site of injury – data that is consistent with a pro–angiogenic microenvironment. sFlt genetic expression rises 2 days after injury, possibly indicating a compensatory response at the genetic level, which is consistent with the vascular regression observed 7 days after injury.
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