April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
Effect of Beta-Adrenergic Receptor and Insulin on IGF-1 Receptor Signaling in Human Retinal Endothelial Cells
Author Affiliations & Notes
  • S. Panjala
    Ophthalmology, Univ of Tennessee Hlth Sci Cntr, Memphis, Tennessee
  • J. J. Steinle
    Ophthalmology, Univ of Tennessee Hlth Sci Ctr, Memphis, Tennessee
  • Footnotes
    Commercial Relationships  S. Panjala, 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, 5622. doi:
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    • Get Citation

      S. Panjala, J. J. Steinle; Effect of Beta-Adrenergic Receptor and Insulin on IGF-1 Receptor Signaling in Human Retinal Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5622.

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

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Purpose: : To determine whether beta-adrenergic receptor stimulation, insulin stimulation or the combined stimulation can regulate IGF-1 receptor signaling in human retinal endothelial cells.

Methods: : Retinal endothelial cells were grown in high glucose medium and treated with xamoterol alone, insulin alone or with both insulin +xamoterol. The treated and non-treated cell lysates were used to examine the role of xamoterol alone, insulin alone, and with both insulin + xamoterol in the regulation of total and phosphorylated IGF-1 receptor, insulin receptor beta, Akt, and caspase 3. TUNEL analyses were done to verify apoptosis.

Results: : Xamoterol reduced IGF-1R, Akt and insulin levels. Insulin significantly increased IGF-1R, Akt, insulin receptor and total insulin levels. Combined treatments increased IGF-1R, Akt and insulin receptor levels in acute treatments, but the response was short. Caspase-3 activity is decreased with all treatments.

Conclusions: : The data suggest that beta-adrenergic receptors and insulin stimulation regulate IGF-1 receptor signaling in retinal endothelial cells. Insulin reduced apoptosis and the cleavage of caspase 3 levels, likely through increased IGF-1 receptor phosphorylation. While xamoterol also reduced apoptosis, this response did not occur through IGF-1 receptor signaling. When insulin and xamoterol treatments are combined, IGF-1 receptor signaling is likely regulated primarily through insulin actions.

Keywords: growth factors/growth factor receptors • neurotransmitters/neurotransmitter systems • diabetic retinopathy 

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