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Hiroto Terasaki, Taro Kamisasanuki, Ken-ichiro Kosai, Taiji Sakamoto; Inhibition Of Choroidal Neovascularization By Targeting To Membrane Protein Cd9. Invest. Ophthalmol. Vis. Sci. 2011;52(14):975.
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© ARVO (1962-2015); The Authors (2016-present)
We previously reported that corneal neovascularization was inhibited by blocking membrane protein CD9, indicating that CD9 plays a pivotal role ocular angiogenesis (ARVO 2010). In the present study, we examined the effect of blocking CD9 on choroidal neovascularization (CNV) in a mouse laser-model and further investigated its therapeutic potential for exudative age-related macular degeneration.
Laser-induced CNV model was produced in C57BL/6 mouse (n=20). CD9 was blocked by inhibitors of either siRNA-CD9 or mouse monoclonal antibody against CD9 (SantaCruz). Each inhibitor was injected into the vitreous on the same day and 7 days after laser shot. On day 14, mice were sacrificed and perfused with FITC-dextran. The size of each CNV was measured by image analyzing system (ImageJ software). Random siRNA was used as a control of siRNA-CD9 and Phosphate buffered saline(PBS) was used as a control of anti-CD9 antibody.
The size of CNV was significantly smaller in siRNA-CD9-treated eyes than controls: the average reduced size was 0.28% vs random siRNA or 0.38% vs PBS). It was also smaller in anti-CD9-treated CNV than in controls (0.013±0.009 mm2 anti-CD9 antibody vs 0.023±0.01 mm2 control, P=0.022, student t test).
Blocking of CD9 resulted in inhibition of laser-induced CNV in mouse. CD9 can be a promising target molecule for the treatment of exudative age-related macular degeneration.
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