May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
COX-2 Promotes VEGF-Induced Angiogenesis in Retinal Endothelial Cells
Author Affiliations & Notes
  • M. L. Clark
    Vanderbilt Univ, Nashville, Tennessee
    Cell and Developmental Biology,
  • Q. Song
    Vanderbilt Univ, Nashville, Tennessee
    Ophthalmology and Visual Sciences,
  • J. M. Barnett
    Vanderbilt Univ, Nashville, Tennessee
  • J. S. Penn
    Vanderbilt Univ, Nashville, Tennessee
    Ophthalmology and Visual Sciences,
  • Footnotes
    Commercial Relationships M.L. Clark, None; Q. Song, None; J.M. Barnett, None; J.S. Penn, Alcon Research, Ltd., C.
  • Footnotes
    Support R01 EY07533-20, T32 HL07411-25, P30 EY08126-14
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 1722. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      M. L. Clark, Q. Song, J. M. Barnett, J. S. Penn; COX-2 Promotes VEGF-Induced Angiogenesis in Retinal Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1722.

      Download citation file:

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

  • Supplements

Purpose:: COX-2, through the induction of prostanoid synthesis, has demonstrated angiogenic activity in cancer models and other contexts. The purpose of the present study was to determine the role of COX-2 in modulating VEGF-induced angiogenic behavior in retinal microvascular endothelial cells (RMEC) and to determine the specific prostanoids responsible.

Methods:: Protein and mRNA were collected from VEGF-treated human RMEC, and COX-2 levels were analyzed by RT-PCR and western blot. Cell lysates and growth medium from VEGF-treated HRMEC were subjected to gas chromatography-mass spectrometry to identify which prostanoids are upregulated by VEGF. HRMEC were transfected with siRNA directed against COX-2 to test for COX-2-dependent VEGF-induced tube formation.

Results:: VEGF treatment of HRMEC increased COX-2 mRNA by 23-fold after 0.5 hours and COX-2 protein by 19-fold after 3 hours, while COX-1 mRNA and protein levels remained constant. Prostanoids PGD2, PGE2, PGF2α, and PGI2 from HRMEC lysates and medium were increased between 1.8- and 4.5-fold at 6 hours of VEGF treatment. The VEGF-induced tube formation was abolished in COX-2 knockdown HRMEC.

Conclusions:: VEGF upregulates COX-2 in HRMEC, leading to increased production of PGD2, PGE2, PGF2α, and PGI2. COX-2, through the action of one or more of these prostanoids, promotes VEGF-induced tube formation, suggesting that prostanoids and their receptors may constitute therapeutic targets in neovascular eye disease.

Keywords: retinal neovascularization • eicosanoids • enzymes/enzyme inhibitors 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.