RIG-I contributes to the innate immune response after cerebral ischemia.

Frank J Brand,Juan Pablo De Rivero Vaccari,Ofelia F Alonso,Juan Carlos De Rivero Vaccari,Nancy H Mejias

doi:10.1186/s12950-015-0101-4

Frank J Brand, Juan Pablo De Rivero Vaccari + Show 3 more

Open Access

https://doi.org/10.1186/s12950-015-0101-4

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Journal: Journal of Inflammation	Publication Date: Sep 14, 2015
Citations: 37	License type: CC BY 4.0

Affiliation: University of Miami, Neurological Surgery

Abstract

BackgroundFocal cerebral ischemia induces an inflammatory response that when exacerbated contributes to deleterious outcomes. The molecular basis regarding the regulation of the innate immune response after focal cerebral ischemia remains poorly understood.MethodsIn this study we examined the expression of retinoic acid-inducible gene (RIG)-like receptor-I (RIG-I) and its involvement in regulating inflammation after ischemia in the brain of rats subjected to middle cerebral artery occlusion (MCAO). In addition, we studied the regulation of RIG-I after oxygen glucose deprivation (OGD) in astrocytes in culture.ResultsIn this study we show that in the hippocampus of rats, RIG-I and IFN-α are elevated after MCAO. Consistent with these results was an increased in RIG-I and IFN-α after OGD in astrocytes in culture. These data are consistent with immunohistochemical analysis of hippocampal sections, indicating that in GFAP-positive cells there was an increase in RIG-I after MCAO. In addition, in this study we have identified n-propyl gallate as an inhibitor of IFN-α signaling in astrocytes.ConclusionOur findings suggest a role for RIG-I in contributing to the innate immune response after focal cerebral ischemia.

Highlights

Focal cerebral ischemia induces an inflammatory response that when exacerbated contributes to deleterious outcomes
Brand et al Journal of Inflammation (2015) 12:52 we show the effects of oxygen glucose deprivation (OGD) on retinoic acid-inducible gene (RIG)-I signaling activation in astrocytes and identify n-propyl gallate as an inhibitor of IFN-α in astrocytes
RIG-like receptors (RLRs) signaling protein expression is altered in the hippocampus of rats after middle cerebral artery occlusion (MCAO) To determine if RLR protein expression is altered after MCAO, we analyzed protein lysates obtained from the hippocampus of rats at different time points after ischemia (1 h, 4 h, 1d and 3d) and in sham-operated animals for the expression of retinoic acid-inducible gene-I (RIG-I) and IFN-α (Fig. 1)

Summary

Introduction

Focal cerebral ischemia induces an inflammatory response that when exacerbated contributes to deleterious outcomes. The molecular basis regarding the regulation of the innate immune response after focal cerebral ischemia remains poorly understood. Stroke is a major problem affecting populations worldwide. It is the second most common cause of death in the world after heart disease. Inflammation is a major contributor to the deleterious effects that present after an ischemic event such as stroke [2]. A component of inflammation is the innate immune response, which is characterized by the activation of pattern recognition receptors (PRR) such as Tolllike receptors (TLRs), NOD-like receptors (NLRs) or RIG-like receptors (RLRs). TLRs have been previously studied in regards to their deleterious and beneficial

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