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

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

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Background: 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. Methods: In 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. Results: In 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. Conclusion: Our findings suggest a role for RIG-I in contributing to the innate immune response after focal cerebral ischemia.

Original languageEnglish (US)
Article number52
JournalJournal of Inflammation (United Kingdom)
Issue number1
StatePublished - Sep 14 2015


  • Innate immunity
  • Neuroinflammation
  • RIG-I
  • Stroke
  • ischemia

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology


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