SARI prevents ocular angiogenesis and inflammation in mice

Abstract

SARI (Suppressor of AP-1, regulated by IFN-β) is known to play an important role in some systemic disease processes such an inflammatory conditions and cancer. We hypothesize that SARI may also play a role in ocular diseases involving inflammation and neovascularization. To explore our hypothesis, further, we investigated an endotoxin-induced uveitis (EIU) and experimental argon laser-induced choroidal neovascularization (CNV) model in SARI wild-type (SARI^WT ) and SARI-deficient (SARI^-/- ) mice. Through imaging, morphological and immunohistochemical (IHC) studies, we found that SARI deficiency exacerbated the growth of CNV. More VEGF-positive cells were presented in the retina of SARI^-/- mice with CNV. Compared to SARI^WT mice, more inflammatory cells infiltrated the ocular anterior segment and posterior segments in SARI^-/- mice with EIU. Collectively, the results point to a potential dual functional role of SARI in inflammatory ocular diseases, suggesting that SARI could be a potential therapy target for ocular inflammation and neovascularization.

Keywords: Suppressor of AP-1; Uveitis; age-related macular degeneration; choroidal neovascularization; regulated by IFN-β; vascular endothelial growth factor.