Beta-adrenergic receptor agonist decreases VEGF levels through altered eNOS and PKC signaling in diabetic retina. (June 2015)

• Record Type: Journal Article
• Authors: Jiang, Youde; Zhang, Qiuhua; Steinle, Jena J.
• Is Part Of: Growth factors. Volume 33:Number 3(2015:Jun.)
• Page Start: 192
• Page End: 199
• Publication Date: 2015-06
• Subjects: Growth factors -- Periodicals; Physiology -- Periodicals; 611
• Languages: English
• ISSNs: 0897-7194

Abstract

<abstract> <title>Abstract</title> <p>Vascular endothelial cell growth factor (VEGF) is increased in diabetic macular edema. Compound 49b, a novel β-adrenergic receptor agonist, is protective in a type 1 diabetic rat model. We questioned whether Compound 49b could decrease VEGF levels, suggesting that Compound 49b may be effective against edema. Two-month diabetic rats received topical Compound 49b for 7 days only and/or insulin-like growth factor binding protein 3 (IGFBP-3) siRNA. We also measured endothelial nitric oxide synthase (eNOS) and protein kinase C (PKC)ζ and PKCδ phosphorylation. Retinal endothelial cells (RECs) cultured in high glucose were treated with Compound 49b and IGFBP-3 siRNA for evaluation of the same signaling pathways. Compound 49b significantly decreased VEGF through increased IGFBP-3 in the diabetic retina. Compound 49b also reduced eNOS, PKCζ and PKCδ phosphorylation in the diabetic retina and REC. Compound 49b regulated a number of proteins involved in REC barrier properties.</p> </abstract>