May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Human Glaucomatous Retinal Ganglion Cells in vitro : Intrinsic Inability for Neuritogenesis?
Author Affiliations & Notes
  • D.M. Bonnet
    Lab Retinal Cellular and Molecular Pathology, INSERM U592, Strasbourg, France
  • G. Hageman
    Center for Macular Degeneration, U. Iowa, Coralville, IA
  • J. Sahel
    Lab Retinal Cellular and Molecular Pathology, INSERM U592, Paris, France
  • D. Hicks
    Lab Retinal Cellular and Molecular Pathology, INSERM U592, Strasbourg, France
  • Footnotes
    Commercial Relationships  D.M. Bonnet, None; G. Hageman, None; J. Sahel, None; D. Hicks, None.
  • Footnotes
    Support  AHAF/ National Glaucoma Research Grant G2002015; grant from the Fédération des Aveugles de France
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 168. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      D.M. Bonnet, G. Hageman, J. Sahel, D. Hicks; Human Glaucomatous Retinal Ganglion Cells in vitro : Intrinsic Inability for Neuritogenesis? . Invest. Ophthalmol. Vis. Sci. 2005;46(13):168.

      Download citation file:


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

      ×
  • Supplements
Abstract

Abstract: : Purpose: Retinal ganglion cell (RGC) neuroprotection can be partly achieved in cell and animal models with several growth factors, including FGF9 and BDNF. The present study was designed to examine in vitro characteristics of aged normal and glaucomatous RGC and to extend studies on neuroprotection of rodent cell culture models. Methods: Fresh human retinas were obtained from post–mortem eyes of informed donors through the Iowa Eye Bank. Human and PN7 rat retina cell cultures were prepared to study RGC survival and regeneration in vitro. Cells were treated by recombinant proteins (FGF9, BDNF) during cell culture and after fixation, we analysed the number and neurite length of neurofilament–immunolabeled RGC. Results: In neonatal rat retinal cell preparations, FGF9 treatment permitted survival of significantly more RGC in both control conditions and under excitotoxic stress (100–500µM glutamate). In normal aged human retinal cell cultures, RGC generated extensive neurites, but we did not observe further stimulation by BDNF. In glaucomatous human cell culture, there was very little spontaneous RGC neuritogenesis and FGF9 did not influence RGC survival. Conclusions: The ability of FGF9 to protect adult pig RGC was also found in an in vitro model of rat retina, and was able to partially overcome glutamatergic excitotoxicity. The capacity of BDNF to stimulate RGC neurite extension was observed in cell cultures derived from animal but not human tissue. In addition, it seems that the spontaneous regrowth of neurites in vitro is compromised in human glaucomatous RGC, suggesting that the residual RGC may be damaged and unable to generate processes.

Keywords: neuroprotection • retinal culture • retinal degenerations: cell biology 
×
×

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.

×