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