Purchase this article with an account.
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)
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.
This PDF is available to Subscribers Only