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Is inhibition of VEGF165 sufficient to inhibit scar formation after trabeculectomy?
Author(s) -
VAN BERGEN T,
VAN DE VEIRE S,
VANDEWALLE E,
MOONS L,
STALMANS I
Publication year - 2009
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2009.2442.x
Subject(s) - pegaptanib , trabeculectomy , in vivo , medicine , bevacizumab , neovascularization , pharmacology , in vitro , ophthalmology , inflammation , angiogenesis , glaucoma , chemistry , surgery , cancer research , immunology , ranibizumab , biology , biochemistry , chemotherapy , microbiology and biotechnology
Purpose We have previously shown that VEGF plays a role in scar formation after glaucoma surgery and that inhibition of all VEGF‐isoforms by bevacizumab is able to reduce scar formation. This study was designed to elucidate the exact role of VEGF165 in scar formation after trabeculectomy. The effect of pegaptanib (Pfizer), which specifically blocks VEGF165, was investigated in vitro and in vivo. Methods The effect of pegaptanib on Tenon fibroblasts and HUVEC in vitro was determined using a WST‐1 proliferation assay. The effect of the aptamer was also investigated in vivo in a rabbit model for glaucoma surgery by studying angiogenesis, inflammation and collagen deposition. Results A dose‐dependent reduction of HUVEC proliferation was seen after pegaptanib administration in vitro (P<0.05 with a dose of at least 0,3 mg/ml). A concentration of 2 mg/ml pegaptanib was necessary to inhibit the proliferation of Tenon fibroblasts. The aptamer also significantly reduced blood vessel density 3 days after surgery in a rabbit model of trabeculectomy (P=0.001). There were no significant differences in inflammation and collagen deposition in the treated eyes compared to control. Conclusion Whereas HUVEC cells were inhibited by pegaptanib in a dose‐dependent way, Tenon fibroblasts were only inhibited at the highest dose. A single administration of pegaptanib at the time of trabeculectomy reduced postoperative angiogenesis, but not inflammation or collagen deposition. Further studies using repeated pegaptanib injections are necessary to investigate whether the lack of effect of pegaptanib on scarring was due to a shorter working time of pegaptanib compared to bevacizumab, or due to the difference in their effect on the various VEGF isoforms.