June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Stimulation of Semaphorin3E/PlexinD1 pathway has anti-angiogenic effect in experimental model of choroidal neovascularization
Author Affiliations & Notes
  • Kenji Suda
    Ophthalmology, Kyoto University, Kyoto, Japan
  • Congrong Guo
    Ophthalmology, Kyoto University, Kyoto, Japan
  • Akio Oishi
    Ophthalmology, Kyoto University, Kyoto, Japan
  • Shinya Ikeda
    Ophthalmology, Kyoto University, Kyoto, Japan
  • Nagahisa Yoshimura
    Ophthalmology, Kyoto University, Kyoto, Japan
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 4580. doi:
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      Kenji Suda, Congrong Guo, Akio Oishi, Shinya Ikeda, Nagahisa Yoshimura; Stimulation of Semaphorin3E/PlexinD1 pathway has anti-angiogenic effect in experimental model of choroidal neovascularization. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4580.

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

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Abstract

Purpose: To prove and investigate the inhibitory effects of Semaphorin3E/PlexinD1 pathway in the development ofchoroidal neovascularization (CNV).

Methods: Methods: We created laser-induced model in c57BL/6 mice. The eyes were enucleated 5 days after laser photocoagulation and the presence and localization of PlexinD1 was investigated with immunochemistry. We obtained mRNA from RPE-choroid-retina complex and the expression of Semaphorin3E and PlexinD1 was investigated with RT-PCR, 1, 3, 5, or 7 days after laser photocoagulation. In addition, we performed the intravitreal injection (IV) of Semaphorin3E 0.1μg (n=9), VEGF Fc 2μg (n=5), or BSA 0.1μg (n=6) soon after the laser photocoagulation and measured the size of CNVs at day 7.

Results: The presence of PlexinD1 was confirmed immunohistochemically with the localization at the edge of CNV. The expression of PlexinD1 mRNA was elevated after the photocoagulation with its peak at day 5 (1.72 times as day 0, P = 0.009). In contrast, the expression of Semaphorin3E mRNA on day 5 was reduced (0.38 times as day 0, P = 0.006). The average size of CNVs was 16320.9 ± 8316.0 μm2 in BSA arm and 9487.4 ± 4424.1 μm2 in Semaphorin3E arm, indicating that Semaphorin3E inhibited the CNV formation significantly (P < 0.01). The average size of CNVs after IV of VEGF Fc was 8091.6 ± 3947.6 μm2. There was no significant difference between Semaphorin3E and VEGF Fc.

Conclusions: This study indicates that Semaphorin3E/PlexinD1 signaling pathway is involved in the formation of CNV and modulation of the pathway might have inhibitory effect for the pathological change. The result might pave the way for a novel treatment strategy for the disease with CNV, e.g.wet age-related macular degeneration.

Keywords: 412 age-related macular degeneration  
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