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Eun Kyoung Lee, Young Joo Kim, Baek-Lok Oh, Hyeong Gon Yu; Inhibition of Experimental Choroidal Neovascularization by Telomerase-derived Peptide GV1001. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2291.
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This study was undertaken to investigate the suppressing effects of a reverse-transcriptase-subunit of telomerase (hTERT) derived peptide, GV1001, on choroidal neovascularization (CNV) in a laser-induced rat model.
The CNV was induced by 577 nm diode laser photocoagulation in a total of 52 male Brown Norway rats. GV1001 (0.1-, 1-, or 10 nM) or vehicle was subcutaneously administered beginning 3 days before and once daily after laser photocoagulation. Fourteen days after laser injury, spectral-domain optical coherence tomography (SD-OCT) and fluorescein angiography (FA) were performed in vivo to evaluate the thickness and leakage of CNV. Choroidal flat mount and histological analysis were conducted to observe the CNV in vitro.
The CNV thickness in GV1001-treated rats was significantly lower than in vehicle-treated rats by histological analysis. The CNV thickness was 48.73 ± 9.30 µm in 0.1nM group (P < 0.001), 43.07 ± 10.40 µm in 1nM group (P < 0.001), 51.50 ± 12.74 µm in 10nM group (P = 0.002), and 68.81 ± 23.14 µm in the control group. The proportion of CNV lesions with clinically significant fluorescein leakage were 37.9%, 21.1%, and 21.4% in rats treated with 0.1-, 1-, and 10 nM of GV1001, respectively, which were significantly lower than in control rats (66.1%, P < 0.001) (Figure 1).
GV1001 suppressed laser-induced CNV formation in rats, especially at 1nM concentration. Further study is needed to identify the mechanism responsible for this CNV inhibitory activity of GV1001.
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