March 2012
Volume 53, Issue 14
ARVO Annual Meeting Abstract  |   March 2012
Suramab Strongly Inhibits Neovascularization Through Downregulation of VEGF, FGF and P2X2 receptor
Author Affiliations & Notes
  • Emiliano S. Lopez
    Research Area, Universidad Austral, Capital Federal, Argentina
  • Juan O. Croxatto
    Eye Pathology, Fundacion Oftalmol Argentina J Malbran, Ciudad de Buenos Aires, Argentina
  • Juan E. Gallo
    Ophthalmology, Hospital Universitario Austral, Pilar, Argentina
  • Footnotes
    Commercial Relationships  Emiliano S. Lopez, None; Juan O. Croxatto, None; Juan E. Gallo, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2400. doi:
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      Emiliano S. Lopez, Juan O. Croxatto, Juan E. Gallo; Suramab Strongly Inhibits Neovascularization Through Downregulation of VEGF, FGF and P2X2 receptor. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2400.

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

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Purpose: : To analyze the role of VEGF, bFGF and P2X2 receptor in the antiangiogenic mechanism of suramab in a rabbit model of corneal neovascularization.

Methods: : Corneal NV was induced in three groups of nine White New Zealand rabbits, applying a filter paper disc soaked in 1M Na (OH) on the central cornea. Group 1 was treated after injury with intravenous Suramab (S) at a dosis equivalent to 3mg/kg of Bevacizumab and 10mg/kg of Suramin, Group 2 was treated with intravenous Bevacizumab (B) at a dosis of 3mg./kg, and Group 3 did not receive any treatment. Animals were sacrificed at 35 days post-injury. Western blot was used to analyze VEGF, bFGF and P2X2 protein expression.

Results: : The presence of VEGF, bFGF and P2X2 proteins was significantly reduced in animals treated with Suramab at 35 days postinjury. This group of animals had much less corneal neovascularization than that found in the other groups.

Conclusions: : Suramab strongly inhibits corneal angiogenesis through downregulation of VEGF, bFGF and P2X2 proteins expression.

Keywords: cornea: clinical science • neovascularization • growth factors/growth factor receptors 

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