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