May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Characterization of the Laser-Induced Choroidal Neovascularization in Apoptosis Modified Mice
Author Affiliations & Notes
  • T. Hisatomi
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
    Ophthalmology, Kyushu University, Fukuoka, Japan
  • S. Nakao
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
    Ophthalmology, Kyushu University, Fukuoka, Japan
  • K. Noda
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • T. Nakazawa
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • L. Almulki
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • Y. Ito
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • H. She
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • T. Ishibashi
    Ophthalmology, Kyushu University, Fukuoka, Japan
  • A. Hafezi-Moghadam
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • J. W. Miller
    Angiogenesis, Mass Eye & Ear Infirmary-Harvard, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  T. Hisatomi, None; S. Nakao, None; K. Noda, None; T. Nakazawa, None; L. Almulki, None; Y. Ito, None; H. She, None; T. Ishibashi, None; A. Hafezi-Moghadam, None; J.W. Miller, None.
  • Footnotes
    Support  National Eye Institute Grant EY014104
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 517. doi:https://doi.org/
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      T. Hisatomi, S. Nakao, K. Noda, T. Nakazawa, L. Almulki, Y. Ito, H. She, T. Ishibashi, A. Hafezi-Moghadam, J. W. Miller; Characterization of the Laser-Induced Choroidal Neovascularization in Apoptosis Modified Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):517. doi: https://doi.org/.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : Laser-injury choroidal neovascularization (CNV) in mice, rats and primates models angiogenic diseases such as age-related macular degeneration. In CNV, robust infiltration of inflammatory cells and endothelial cells take place into the laser-injured site, however these cells gradually diminish over time. Apoptotic cell death may be involved, but the mechanism remains unclear.

Methods: : To elucidate the role of apoptosis in CNV, we quantified CNV formation in wild type (WT) and apoptosis inducing factor (AIF) mutant mice (AIF-/Y). CNV was induced by laser photocoagulation with 532nm, 150mW, 100msec, 50µm settings. Eyes were enucleated at 1, 2, 4, and 12 weeks of age and were analyzed using immunohistochemistry, TUNEL, transmission electron microscopy (TEM), RT-PCR and western blotting. To test macrophage apoptosis, peritoneal macrophages induced by thioglycollate medium were collected from AIF-/Y and WT mice and cultured under starved conditions for 24 hours.

Results: : CNV size was increased in AIF-/Y mice compared to WT in 2, 4, 12 weeks after laser induction. Following laser injury, inflammatory / endothelial apoptosis detected by TUNEL was significantly lower in AIF deficient mice when compared to WT at 4 weeks. The AIF-/Y peritoneal macrophages showed less apoptosis compared to WT in culture under starved conditions.

Conclusions: : Mice lacking AIF show substantial persistence of inflammatory / endothelial cells at the laser-injury site. Our data suggest that apoptosis plays an important role in laser-induced CNV, and therapeutic modulation of apoptosis via AIF may offer a new target for treatment of CNV.

Keywords: choroid: neovascularization • apoptosis/cell death • laser 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×