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Youde Jiang, Jena J Steinle; Epac1 is required for Beta-Adrenergic Receptor Regulation of VEGF in Retinal Endothelial Cells Grown in High Glucose. Invest. Ophthalmol. Vis. Sci. 2016;57(12):3212.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether Compound 49b, a novel beta-adrenergic receptor agonist, significantly decreases VEGF levels through Epac1 actions in human retinal endothelial cells (REC) grown in high glucose.
REC were grown in normal (5mM) or high (25mM) glucose for 3 days. Some cells were transfected with Epac1 siRNA and/or treated with Compound 49b. Western blotting and ELISA analyses were done to measure Epac1, VEGF, IGFBP-3, PKCzeta, and cleaved caspase 3 levels
High glucose significantly increased VEGF, PKCzeta and cleaved caspase 3 levels, while reducing Epac1 and IGFBP-3. Compound 49b significantly reduced VEGF levels, PKCzeta and cleaved caspase 3 levels, while increasing Epac1 and IGFBP-3. The actions of Compound 49b on VEGF, PKCzeta, and caspase 3 were inhibited when Epac1 siRNA was used.
The results suggest that Compound 49b activates Epac1 to regulate VEGF signaling in REC, leading to reduced permeability and apoptosis. These data provide novel upstream pathways of VEGF that can potentially be used for novel therapies.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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