April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Interleukin 17 Stimulates STAT3-dependent VEGF Expression in Retinal Endothelial Cells
Author Affiliations & Notes
  • Ajay Pillai
    Ophthalmology,
    Medical College of Georgia, Augusta, Georgia
  • Anna Lisa Montemari
    Fondazione GB Bietti, Rome, Italy
  • Chaunte Stampley
    Ophthalmology,
    Medical College of Georgia, Augusta, Georgia
  • Curran Dalal
    Ophthalmology,
    Medical College of Georgia, Augusta, Georgia
  • Folami Lamoke
    Department of Ophthalmology, Pharmacology and Toxicology,
    Medical College of Georgia, Augusta, Georgia
  • Babak Baban
    Oral Biology and Maxillofacial Pathology,
    Medical College of Georgia, Augusta, Georgia
  • Manuela Bartoli
    Department of Ophthalmology, Pharmacology and Toxicology,
    Medical College of Georgia, Augusta, Georgia
  • Footnotes
    Commercial Relationships  Ajay Pillai, None; Anna Lisa Montemari, None; Chaunte Stampley, None; Curran Dalal, None; Folami Lamoke, None; Babak Baban, None; Manuela Bartoli, None
  • Footnotes
    Support  Vision Discovery Institute, Department of Ophthalmology, Medical College of Georgia
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 3547. doi:
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      Ajay Pillai, Anna Lisa Montemari, Chaunte Stampley, Curran Dalal, Folami Lamoke, Babak Baban, Manuela Bartoli; Interleukin 17 Stimulates STAT3-dependent VEGF Expression in Retinal Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3547.

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

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Abstract

Purpose: : Interleukin 17 (IL-17) is an inflammatory cytokine which has been shown to be involved in chronic inflammatory diseases. Our previous studies have shown that circulating (serum) levels of IL-17 are increased in diabetic patients presenting signs of macular edema and neovascularization. To better understand IL-17’s mode of action we determined its effects in inducing VEGF expression in isolated retinal endothelial cells (RECs).

Methods: : RECs, of bovine and human origins, were stimulated for different times (5,15,30,60,90 minutes) with different doses (1, 10, 50, 100 ng/mL) of IL-17A or IL-17F. Other experiments were conducted by stimulating RECs with 50ng/mL of IL-17A and IL-17F for 1, 6, 12 and 24 hours. Western blotting analysis was carried out to determine activation/phosphorylation of signal transducer and activator of transcription 3 (STAT3) and protein levels of VEGF. Small interfering RNAs-induced selective blockade of STAT3 expression was also used (by transfecting RECs) to determine direct cause-effect relationship between activation of STAT3 and IL-17-induced VEGF expression.

Results: : Stimulation of RECs with both IL-17F and A resulted in a time and dose dependent effect on activation/phosphorylation of STAT3. As a result of STAT3 activation, we observed increased VEGF expression which was detectable at 6 hours and peaked at 12 hours post-treatment. Inhibition of STAT3 expression by siRNAs in RECs blunted IL-17 -induced VEGF expression.

Conclusions: : Our results suggest that IL-17 stimulates VEGF expression in RECs. These data may explain our previous observations of up-regulation of IL-17 in diabetic patients affected by macular edema and proliferative diabetic retinopathy.

Keywords: diabetic retinopathy • vascular endothelial growth factor • edema 
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