The role of CB2 receptors in proliferative vitreoretinopathy

Abstract

Proliferative vitreoretinopathy (PVR) is known to be the most common sight-seeing complication of retinal detachment. The pathogenesis of PVR is characterized by the proliferation and migration of retina pigmented epithelial cells, which leads to formation of contractile cellular membranes and retinal breaks, as well as immune cell infiltration. The Endocannabinoid system modulates immune response; cannabinoid receptor 2 (CB2) is expressed in the cells of the immune system, but also found in the retina. The activation of the CB2 receptor by endogenous or exogenous ligands produces biological activities of immune function; the expression of this receptor is up-regulated by the activation of various inflammatory triggers. The purpose of this study is to further understand what role the CB2 receptor plays during inflammation in the retina and if it is involved in the mediation of immunosuppressive effects. An animal model (mice) was used to induce PVR with an intraocular injection (0.2μl) of 0.1U dispase, a proteolytic enzyme. The severity of PVR in wild type (WT) and CB2-/- saline and dispase groups were evaluated through the observation of cross-sectioned H&E stained ocular tissues. IL-1[beta] cytokine concentrations were captured using an enzyme linked immunosorbent assay with IL-1[beta] sensitive antibodies. Histological H&E staining demonstrated pronounced ocular damage in CB2-/- animals compared to WT animals. IL-1[beta] cytokine concentrations showed no significant difference (p>0.05) between WT and CB2-/- animals. From the results, the ocular damage was more pronounced in CB2-/- mice as compared to WT mice, which suggests an immunodulatory role for CB2 receptors.