April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Novel Beta-Adrenergic Receptor Agonist Prevents Retinal Endothelial Cell Death Through Increased IGFBP3 Levels
Author Affiliations & Notes
  • Qiuhua zhang
    Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee
  • Youde Jiang
    Ophthalmology, UT Health Science Center, Memphis, Tennessee
  • Robert Ferry
    Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee
  • Jena J. Steinle
    Ophthalmology and Anatomy&Neurobiology, Univ of Tennessee Hlth Sci Ctr, Memphis, Tennessee
  • Footnotes
    Commercial Relationships  Qiuhua zhang, None; Youde Jiang, None; Robert Ferry, None; Jena J. Steinle, None
  • Footnotes
    Support  JDRF CDA 2006-144, JDRF 2008-1044, RPB Special Scholar's Award, RPB Deparmental Award, NIH PHS 3P30 EY013080, NIH 5U01 DK085465-02 (RF, PI in Memphis)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 3583. doi:
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    • Get Citation

      Qiuhua zhang, Youde Jiang, Robert Ferry, Jena J. Steinle; Novel Beta-Adrenergic Receptor Agonist Prevents Retinal Endothelial Cell Death Through Increased IGFBP3 Levels. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3583.

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

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Abstract

Purpose: : To determine whether Compound 49b, a novel β-adrenergic receptor agonist, increases IGFBP3 levels to inhibit apoptosis in the diabetic retina.

Methods: : Male rats were made diabetic with a single injection of streptozotocin (60mg/kg). Three groups of rats were used: control, diabetic, and diabetic+Compound 49b treated. Compound 49b eye drops (1 mM) were administered daily. After 8 months of treatment, retinal protein levels of IGFBP-3, Bad, Fas, Fas ligand, and Bcl-xl, and cleaved caspase 3 levels were measured by Western blot or ELISA.

Results: : Compound 49b eye drops increased IGFBP3 levels (P<0.05 vs. untreated diabetic). Concurrent with the increase in IGFBP3, Compound 49b treatment significantly decreased levels of key pro-apoptotic markers Bad, Fas, Fas ligand, and cleaved caspase 3 (P<0.05 vs untreated diabetic retina).

Conclusions: : A novel β-adrenergic receptor agonist, Compound 49b, can significantly increase IGFBP3 levels in the diabetic retina, while decreasing key pro-apoptotic markers. This is the first demonstration of regulation of IGFBP3 by β-adrenergic receptor agonists, as well as a potential anti-apoptotic mechanism for IGFBP3. Future studies will investigate the mechanism by which native IGFBP3 may inhibit retinal endothelial cell death.

Keywords: apoptosis/cell death • diabetic retinopathy • signal transduction 
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