April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Novel Beta Adrenergic Receptor Agonist in the Treatment of Diabetic Retinopathy
Author Affiliations & Notes
  • K. P. Williams
    Ophthalmology,
    Univ of Tennessee Hlth Sci Center, Memphis, Tennessee
  • J. Pagadala
    Ophthalmology,
    Univ of Tennessee Hlth Sci Center, Memphis, Tennessee
  • D. D. Miller
    Pharmaceutical Sciences,
    Univ of Tennessee Hlth Sci Center, Memphis, Tennessee
  • J. J. Steinle
    Ophthalmology, Univ of Tennessee Hlth Sci Ctr, Memphis, Tennessee
  • Footnotes
    Commercial Relationships  K.P. Williams, None; J. Pagadala, None; D.D. Miller, None; J.J. Steinle, None.
  • Footnotes
    Support  CDA JDRF 2-2006-114, JDRF Translational Award 17-2008-1044, William and Mary Greve Special Scholars Award RPB, P30EY013080 (PI: Dianna Johnson), RPB (PI:Barrett Haik)
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5630. doi:https://doi.org/
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    • Get Citation

      K. P. Williams, J. Pagadala, D. D. Miller, J. J. Steinle; Novel Beta Adrenergic Receptor Agonist in the Treatment of Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5630. doi: https://doi.org/.

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

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Abstract

Purpose: : The goal of this study was to test whether a novel beta-adrenergic receptor agonist can reduce apoptosis and TNFα in vitro. This agent will also be used topically for chronic studies of diabetic retinopathy.

Methods: : Retinal endothelial cells and Müller cells were cultured in high glucose (25mM) media. Cells were treated with various novel beta-adrenergic receptor agonists at specific dosages and time points. Cells receiving no treatment served as controls. Caspase-3 ELISA and TNF-α ELISAs were performed to evaluate apoptosis and inflammatory markers. Two-month diabetic rats were treated for 4 days with compound 49b, followed by PKA ELISA and CREB Western blotting to optimize the dose of 49b.

Results: : Compound 49b significantly reduced caspase-3 and TNF-α levels in both cell types. Caspase-3 and TNF-α levels were significantly reduced at 50nM in cultured cells, a dose lower than that of a non-specific beta-adrenergic agonist, isoproterenol. PKA levels were significantly increased in diabetic rats treated with 49b at a dose of 10mM.

Conclusions: : These results indicate that a novel beta-adrenergic receptor agonist is able to reduce inflammation and cell death, common features of non-proliferative diabetic retinopathy. The topical application of the novel compound is currently being tested in vivo in chronic diabetes at 10mM. We will assess diabetic-like changes at 2 and 8-months following treatment.

Keywords: neurotransmitters/neurotransmitter systems • apoptosis/cell death • inflammation 
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