May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Aspirin-Triggered Lipoxin Agonist (ATLa) Inhibits Corneal Angiogenesis
Author Affiliations & Notes
  • Y. Jin
    Department of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts
  • M. Arita
    Department of Anesthesiology, Perioperative and Pain Medicain, The Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical school, Boston, Massachusetts
  • Q. Zhang
    Department of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts
  • C. Serhan
    Department of Anesthesiology, Perioperative and Pain Medicain, The Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical school, Boston, Massachusetts
  • R. Dana
    Department of Ophthalmology, Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts
  • Footnotes
    Commercial Relationships Y. Jin, None; M. Arita, None; Q. Zhang, None; C. Serhan, None; R. Dana, None.
  • Footnotes
    Support NIH EY-RO1-12963
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 199. doi:https://doi.org/
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    • Get Citation

      Y. Jin, M. Arita, Q. Zhang, C. Serhan, R. Dana; Aspirin-Triggered Lipoxin Agonist (ATLa) Inhibits Corneal Angiogenesis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):199. doi: https://doi.org/.

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

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Abstract

Purpose:: Aspirin-triggered lipoxin (ATL) evokes bioactions in a range of physiologic and pathophysiologic processes and serves as an endogenous lipid/chemical mediator that has been shown in several tissues to reduce neutrophilic infiltration and initiate resolution of inflammation. Here, we investigated the impact of an ATL stable agonist, ATLa, on corneal angiogenesis.

Methods:: The suture-induced model of corneal angiogenesis was used in this study. ATLa (100ng /10µl) was injected subconjunctivally every 48 hours after intrastromal sutures were placed in the corneas. The vehicle alone was used as a negative control. After 72 hours, the expression of TNF-α, IL-1α, IL-1ß, and VEGF ligands and their receptors in the cornea was detected by quantitative real-time PCR. Inflammatory cell infiltration was assayed by Gr-1+ staining on corneal cross-sections. After two weeks of observation, the vascularized areas were analyzed morphometrically on CD31-LYVE-1-double-stained corneal flatmounts (blood vessels = CD31hiLYVE-1-).

Results:: After 72 hours, ATLa-treated eyes demonstrated reduced levels of TNF-α, IL-1α, IL-1ß, VEGF and VEGFR2 expression compared to the control group. However, in contrast to what has been reported for other tissues, the difference in the level of Gr-1 + cell infiltration between the two groups did not reach statistical significance (P=0.06). After two weeks, the angiogenic response in ATLa-treated corneas (13.0% ± 3.81%) was significantly (54.5%) lower than in vehicle-treated corneas (28.6% ± 6.76%; P=0.002, n=6).

Conclusions:: Our results suggest that ATLa-mediated responses can significantly suppress corneal angiogenesis via inhibiting inflammatory cytokines and VEGF /VEGFR2 expression in the inflamed corneal tissue.

Keywords: neovascularization • immunomodulation/immunoregulation • cornea: basic science 
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