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G. E. Lang, S. Lang, H. L. Deissler; Ranibizumab Restored VEGF-Induced Stimulation of iBREC Proliferation and Migration. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2647. doi: https://doi.org/.
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Because VEGF signalling is deregulated in diabetic retinopathy, potential therapeutic effects of VEGF-inhibitors like the humanised VEGF-specific antibody ranibizumab are currently tested in the treatment of diabetic retinopathy. We therefore investigated if VEGF-stimulated processes in retinal endothelial cells were reverted by ranibizumab.
The influence of VEGF and other growth factors on proliferation of immortalised bovine retinal endothelial cells (iBREC) were studied in the presence and absence of ranibizumab. In addition, iBREC migration in the presence of VEGF121 and VEGF165 as well as ranibizumab was investigated.
Proliferation of iBREC which had been significantly stimulated by VEGF121 or VEGF165 at 1 to 100 ng/ml was reduced to basal levels by treatment with 100 µg/ml ranibizumab whereas this Fab fragment did not influence proliferation of unstimulated cells. Concentrations of ranibizumab below 100 µg/ml were not sufficient to revert VEGF121- or VEGF165-stimulated iBREC proliferation. iBREC proliferation stimulated by bFGF was not significantly inhibited by ranibizumab. IGF-1 also slightly stimulated proliferation of iBREC which was in part inhibited by ranibizumab. Only VEGF165 stimulated cell migration in a concentration-dependent manner, whereas VEGF121 and IGF-1 showed no effect. Maximum stimulation was observed at a concentration of 10 ng/ml and addition of 25 µg/ml or 50 µg/ml ranibizumab was sufficient to revert increased iBREC migration induced with 10 ng/ml or 100 ng/ml VEGF165, respectively.
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