June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Serum Autoantibody Evaluation after Retinal Laser Injury in Mice
Author Affiliations & Notes
  • Yannis Paulus
    Ophthalmology, Stanford University, Palo Alto, CA
  • Chuan-Hui Kuo
    Pediatrics, University of Cincinnati, Cincinnati, OH
  • Kei Morohoshi
    Pediatrics, University of Cincinnati, Cincinnati, OH
  • Alex Nugent
    Ophthalmology, Stanford University, Palo Alto, CA
  • Luo Luo Zheng
    Ophthalmology, Stanford University, Palo Alto, CA
  • Hiroyuki Nomoto
    Ophthalmology, Stanford University, Palo Alto, CA
  • Mark Blumenkranz
    Ophthalmology, Stanford University, Palo Alto, CA
  • Daniel Palanker
    Ophthalmology, Stanford University, Palo Alto, CA
  • Santa Ono
    Pediatrics, University of Cincinnati, Cincinnati, OH
  • Footnotes
    Commercial Relationships Yannis Paulus, None; Chuan-Hui Kuo, None; Kei Morohoshi, None; Alex Nugent, None; Luo Luo Zheng, None; Hiroyuki Nomoto, None; Mark Blumenkranz, avalanche biotechnologies (I), avalanche biotechnologies (P), optimedica (I); Daniel Palanker, None; Santa Ono, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 3178. doi:
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      Yannis Paulus, Chuan-Hui Kuo, Kei Morohoshi, Alex Nugent, Luo Luo Zheng, Hiroyuki Nomoto, Mark Blumenkranz, Daniel Palanker, Santa Ono; Serum Autoantibody Evaluation after Retinal Laser Injury in Mice. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3178.

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

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Abstract

Purpose: Laser therapy is an effective treatment modality of several retinal conditions and has been shown to cause dramatic changes locally in heat shock protein expression and other inflammatory markers. This study seeks to characterize the cellular, immunological, and inflammatory response after laser lesions are delivered to the eye, by assessing the changes in serum autoantibodies after very intense retinal photocoagulation.

Methods: Seven C57BL6 mice (8 weeks old) were irradiated using a 532nm laser (PASCAL, Topcon, Santa Clara, CA) with beam diameter of 60 µm, power of 400 mW, and pulse duration of 50 ms to induce 10 laser burns that ruptured Bruch’s membrane per eye. Blood was drawn from the saphenous vein prior to laser treatment and 2 months following laser treatment. The serum was withdrawn from the blood and run on antigen microarrays with 85 molecular markers associated with age-related macular degeneration and other retinal diseases.

Results: Rupture of Bruch’s membrane by laser and likely associated choroidal neovascularization resulted in dramatic changes in the IgG reactivity of autoantibodies 2 months after laser injury. Almost every autoantibody was changed in expression, with approximately two-thirds increasing expression and one-third decreasing expression. Some notable auto-antibodies which were increased dramatically included complement C3, CRP, PKM2, Calretioulin, Collagen V, Collagen VI, SOD1, aldolase, L-glutamine synthetase, annexin II, CNPase, RPE, and Factor X.

Conclusions: Laser injury, specifically intense rupture burns which induce choroidal neovascularization, cause a dramatic change in the serum autoantibody profile after 2 months. Age-related macular degeneration and cancer-associated retinopathy in humans show a similar elevation in serum complement, CEP, α-enolase, and hsp antibodies. Laser-induced choroidal neovascularization could serve as a novel animal model for studying the pathogenesis, immune response, and potential pharmaceutical targets of retinal degenerations.

Keywords: 557 inflammation • 578 laser • 695 retinal degenerations: cell biology  
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