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Graefes Arch Clin Exp Ophthalmol. 2014 Jun;252(6):943-9. doi: 10.1007/s00417-014-2626-2. Epub 2014 Apr 15.

Blockade of the VEGF isoforms in inflammatory corneal hemangiogenesis and lymphangiogenesis.

Author information

1
Department of Ophthalmology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91054, Erlangen, Bavaria, Germany.

Abstract

BACKGROUND:

The VEGF-A family plays a crucial role in the induction of pathological corneal neovascularization. The role of the different VEGF-A isoforms during lymphangiogenesis is only little-known. Current anti-angiogenic therapies in the eye and other organs inhibit all VEGF-A isoforms, and have effects on both blood and lymphatic vessels. Here we investigate whether selective targeting of the isoform VEGF 165 is able to inhibit corneal lymphangiogenesis under inflammatory conditions.

METHODS:

The mouse model of suture-induced corneal neovascularization was used to assess the antihem- and antilymphangiogenic effect of topically applied pegaptanib. Corneal blood and lymph vascularized areas were analyzed morphometrically. Furthermore, we analyzed the proliferative effects of VEGF A 121, 165, and 189 on blood and lymphatic endothelial cells (BEC/LEC) via a cell-proliferation assay.

RESULTS:

Pegaptanib significantly inhibited inflammatory corneal hemangiogenesis (p < 0.01), but not lymphangiogenesis in vivo (p > 0.05), both topically as well as systemically, in the inflamed cornea. In vitro, BECs were more susceptible to pegaptanib than LECs.

CONCLUSIONS:

Targeting VEGF-A 165 significantly inhibits hem- but not lymphangiogenesis, suggesting VEGF-A 165 to be critical for hem-, but dispensable for lymphangiogenesis, at least in the inflamed cornea.

PMID:
24728466
DOI:
10.1007/s00417-014-2626-2
[Indexed for MEDLINE]

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