RIG-I Signaling in the Innate Immune Response After Stroke (INM1P.445)

Abstract

Abstract Stroke is associated with an inflammatory response that contributes to deleterious outcomes. However, the molecular basis in the regulation of inflammation remains poorly understood. Here, we examine the activation of retinoic acid inducible gene-like (RIG) receptors (RLRs) and the involvement of RLR signaling in the regulation of type I IFNs following mid-cerebral artery occlusion (MCAO). In this study we show that in the rat hippocampus RIG-I and IFN-α expression are increased after MCAO. Similarly, we show that in astrocytes in culture, oxygen glucose deprivation (OGD) resulted in increased RIG-I and IFN-α expression. These data are consistent with immunohistochemical analysis of hippocampal sections, indicating that in glial fibrillary acidic protein (GFAP) positive cells there was an increase in RIG-I immunoreactivity after MCAO. Moreover, n-propyl gallate (n-PG) can be used to inhibit RIG-I/IFN-α signaling in astrocytes. In conclusion, these data indicate that RIG-I is involved in the inflammatory response after stroke.