Abstract
Purpose :
The exact mechanisms leading to myopic ocular complications are unclear. VEGF has been suggested to play a key role in myopic choroidal neovascularization (CNV), which can lead to irreversible vision loss. VEGF signals endothelial cells to proliferate and migrate causing neovascularization, and is upregulated during ischemia-related myopic axial elongation. This suggests that VEGF may be a direct trigger of myopic CNV. This study investigates the associations between retinal and choroidal VEGF-A concentrations with myopia development and RPE thickness.
Methods :
Two-month old marmosets (n = 10) wore –5.00 or –10.00 D soft contact lenses for 18 to 38 weeks to induce myopia and axial elongation of various degrees. Refractive error (RE) and axial length (AL) were measured using a Nidek autorefractor and A-scan biometer, respectively, before and after lens treatment. Foveal and parafoveal RPE thickness were measured using optical coherence tomography (OCT) at the end of lens treatment, after which retinal and choroidal VEGF-A concentrations were quantified using ELISA.
Results :
Eyes exhibiting myopia had greater axial elongation (R2 = 0.50, p < 0.001). The degree of eye growth and myopia developed correlated with retinal VEGF-A concentration, such that larger and more myopic eyes exhibited lower retinal VEGF-A concentrations (R2 = 0.27, p = 0.037 and R2 = 0.34, p = 0.009, respectively). There was also a trend towards increased choroidal VEGF-A concentrations in myopic eyes that exhibited thicker nasal parafoveal RPE, but it did not reach significance (R2 = 0.40, p = 0.07).
Conclusions :
VEGF-A concentration changed in marmoset eyes with different degrees of myopia and axial elongation. Low myopic eyes had higher VEGF-A concentrations than high myopic eyes. These differences could be due to a diluting effect caused by increased eye size/volume with a higher turnover rate, or represent an altered physiological production due to sustained RPE cellular stretch.
This is a 2021 ARVO Annual Meeting abstract.