May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Mural Cell Loss Following Inhibition of PDGF Signaling Enhances the Effect of Anti–VEGF Therapy on Corneal Neovascularization
Author Affiliations & Notes
  • N. Jo
    Eyetech Research Center, Lexington, MA
  • C. Mailhos
    Eyetech Research Center, Lexington, MA
  • K. Nishijima
    Eyetech Research Center, Lexington, MA
  • M. Ju
    Eyetech Research Center, Lexington, MA
  • E. Cheung
    Eyetech Research Center, Lexington, MA
  • G.S. Robinson
    Eyetech Research Center, Lexington, MA
  • A.P. Adamis
    Eyetech Research Center, Lexington, MA
  • D.T. Shima
    Eyetech Research Center, Lexington, MA
  • Footnotes
    Commercial Relationships  N. Jo, Eyetech Pharmaceuticals E; C. Mailhos, Eyetech Pharmaceuticals E; K. Nishijima, Eyetech Pharmaceuticals E; M. Ju, Eyetech Pharmaceuticals E; E. Cheung, Eyetech Pharmaceuticals E; G.S. Robinson, Eyetech Pharmaceuticals E; A.P. Adamis, Eyetech Pharmaceuticals E; D.T. Shima, Eyetech Pharmaceuticals E.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 468. doi:
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      N. Jo, C. Mailhos, K. Nishijima, M. Ju, E. Cheung, G.S. Robinson, A.P. Adamis, D.T. Shima; Mural Cell Loss Following Inhibition of PDGF Signaling Enhances the Effect of Anti–VEGF Therapy on Corneal Neovascularization . Invest. Ophthalmol. Vis. Sci. 2005;46(13):468.

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

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Abstract

Abstract: : Purpose: To test whether targeting mural cells (MCs) with a specific PDGF–B signaling inhibitor enhances the effect of anti–VEGF reagents at inhibiting corneal neovascularization (CoNV). Methods: CoNV was induced by removal of the corneal epithelia. Mice were treated with either PDGF–B signaling inhibitors, anti–VEGF aptamer, or both in combination at various time points post–injury. Corneal NV was analyzed using concanavalin A lectin staining to mark the endothelium, smooth muscle actin antibody staining to mark mural cells (MCs), and by electron microscopy for morphological analysis. Results: Inhibition of PDGF–B signaling blocked MC recruitment to newly growing vessels and caused MC detachment from recently established neo–vessels. However, interfering with PDGF–B signaling alone resulted in no significant inhibition of vessel growth. In contrast, blocking VEGF signaling using Macugen TM, an anti–VEGF165 aptamer, was effective at preventing corneal NV, but less effective at regressing established corneal vessels. Macugen efficacy over time, however, was greatly improved by using it in combination with PDGF–blocking reagents capable of disrupting the endothelial/MC interaction. Conclusions: We have found that MC loss following inhibition of PDGF–B signaling enhances the effect of anti–VEGF therapy on corneal NV. Thus, combination therapy using both VEGF and PDGF–B inhibitors could be a more effective treatment for patients with advanced ocular NV.

Keywords: neovascularization • vascular cells • cornea: basic science 
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