May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Neurotrophic Effect of a Novel TrkB Agonist on Retinal Ganglion Cells
Author Affiliations & Notes
  • Y. Hu
    Bascom Palmer Eye Institute, University of Miami Miller School of Med, Miami, Florida
  • S. Cho
    Wyeth Research, Neuroscience Discovery Research, Princeton, New Jersey
  • J. L. Goldberg
    Bascom Palmer Eye Institute, University of Miami Miller School of Med, Miami, Florida
  • Footnotes
    Commercial Relationships  Y. Hu, None; S. Cho, Wyeth conflict of interest, P; J.L. Goldberg, None.
  • Footnotes
    Support  James and Esther King Foundation (JLG), NIH R01 NS061348 (JLG), The Glaucoma Foundation (JLG), NEI P30 EY014801 (UM), and an unrestricted grant from Research to Prevent Blindness (UM).
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5838. doi:https://doi.org/
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    • Get Citation

      Y. Hu, S. Cho, J. L. Goldberg; Neurotrophic Effect of a Novel TrkB Agonist on Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5838. doi: https://doi.org/.

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

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Abstract

Purpose: : Retinal ganglion cells (RGCs) die in glaucoma and a number of other optic neuropathies. Recently, novel TrkB monoclonal antibodies have been shown to be able to activate TrkB receptors and exert neuroprotective and neurotrophic effects. In the present study, we examined the ability of one of these, 29D7, on RGC survival in culture.

Methods: : RGCs from postnatal day (P)3-4 Sprague-Dawley rats were isolated to over 99% homogeneity by sequential immunopanning using a monoclonal antibody to Thy1. RGCs were cultured in 96 well plates pre-coated with poly-D-lysine and laminin at a density of 2x103 cells/well, in serum-free defined medium. RGC viability was assessed after 1-3 days by an MTT assay.

Results: : Similar to BDNF, the 29D7 antibody strongly promoted RGC survival in vitro compared with medium alone or control IgG at 24 hours in culture. Forskolin, which weakly supported RGC survival on its own, potentiated the effect of 29D7.

Conclusions: : These findings demonstrate the potential for antibody-mediated TrkB agonism as a potential therapeutic reagent for treating RGCs after injury or in degenerative disease.

Keywords: neuroprotection • cell survival • pathology: experimental 
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