Cannabinoid (JWH-133) therapy could be effective for treatment of corneal neovascularization

Neovascularization of the normally avascular cornea was associated with a notable increase in the expression of the major proangiogenic factors and proteases. The data supporting a causal role for vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) are extensive. Anti-angiogenic therapy is considered as a possible tool for controlling corneal neovascularization. Endocannabinoids are now considering as suppressors of angiogenesis and tumor spreading since they have been reported to inhibit angiogenesis, cell migration and metastasis in different types of cancers. JWH-133 as a CB2 selective ligand is one of the pharmacological cannabinoid derivatives that could induce apoptosis and reduce secretion of major stimulatory factors involved in cell proliferation and angiogenesis. Several studies have indicated that JWH-133 inhibit tumor angiogenesis in vitro and in vivo through direct inhibition of vascular endothelial cell migration and survival, as well as suppression of proangiogenic factor and MMP-2 expression.Based on the present information about inducing factors involved in corneal angiogenesis and pharmacological properties of cannabinoids, we hypothesize that topical application of JWH-133 is potentially useful for inhibiting corneal neovascularization and restoration of corneal clarity. The potential use of JWH-133 in other eye related reports is even more appealing considering that it could be a good safety profile for retarding corneal neovascularzation. However, further investigations in animal models are needed to place JWH-133 alongside corneal neovascularization therapeutics.