May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
A Potential Role for PDGF–CC in Proliferative Vitreoretinopathy
Author Affiliations & Notes
  • H. Lei
    The Schepens Eye Research Institute & Department of Harvard Medical School, Boston, MA
  • P. Hovland
    The Schepens Eye Research Institute & Department of Harvard Medical School, Boston, MA
  • G. Velez
    The Schepens Eye Research Institute & Department of Harvard Medical School, Boston, MA
  • U. Eriksson
    Ludwig Institute for Cancer Research, Stockholm, Sweden
  • D.G. Gilbertson
    ZymoGenetics Inc, Seattle, WA
  • D.G. Gilbertson
    ZymoGenetics Inc, Seattle, WA
  • T. Hirose
    The Schepens Eye Research Institute & Department of Harvard Medical School, Boston, MA
  • A. Kazlauskas
    The Schepens Eye Research Institute & Department of Harvard Medical School, Boston, MA
  • Footnotes
    Commercial Relationships  H. Lei, None; P. Hovland, None; G. Velez, None; U. Eriksson, None; D.G. Gilbertson, None; D.G. Gilbertson, None; T. Hirose, None; A. Kazlauskas, None.
  • Footnotes
    Support  NIH Grant EY012509
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3828. doi:
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      H. Lei, P. Hovland, G. Velez, U. Eriksson, D.G. Gilbertson, D.G. Gilbertson, T. Hirose, A. Kazlauskas; A Potential Role for PDGF–CC in Proliferative Vitreoretinopathy . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3828.

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

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Abstract

Purpose: : Proliferative vitreoretinopathy (PVR) is a disorder characterized by the formation of cellular membranes on both surfaces of the retina and within the vitreous cavity. It occurs in about 10% of patients that undergo retinal re–attachment surgery. Platelet–derived growth factor (PDGF) receptor α makes an important contribution to the development of PVR in a rabbit model of the disease. The purpose of this study was to test the hypothesis that PDGF–CC (the newly discovered PDGF isoform that activates the PDGF receptor α) contributes to experimental and/or clinical PVR.

Methods: : We analyzed the conditioned medium from fibroblasts (which cause PVR in the experimental model) and retinal pigment epithelial cells (A–RPE19) by PDGF–CC Western blot analysis to test if they secrete PDGF–CC. Since PDGF–CC is secreted in a latent form and must be proteolytically processed to become biologically active, we established a PDGF–CC processing assay and tested conditioned medium from the above–mentioned cells lines for processing activity. Vitreous specimens, from patients undergoing vitrectomy surgery to repair retinal detachment or for other reasons, were also tested for PDGF–CC and processing activity.

Results: : Conditioned medium from both cell lines had readily detectable levels of PDGF–CC and processing activity. At least one of the protease responsible for processing PDGF–CC appeared to be tissue–plasminogen activator (t–PA) because T–PA–STOP a t–PA inhibitor partially blocked processing. PDGF–CC was also present in vitreous of some of the PVR patients. There was also processing activity detected, which was completely blocked by the t–PA inhibitor.

Conclusions: : PDGF–CC is secreted and processed by cells that induce PVR in an experimental model of the disease. Furthermore, both PDGF–CC and the enzymes that convert it to its biologically active form are present in the vitreous of PVR patients. These findings support the idea that one of the new PDGF family members contribute to experimental and clinical PVR.

Keywords: proliferative vitreoretinopathy • vitreous • growth factors/growth factor receptors 
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