Strawberry notch homolog<em> 2</em> gene expression is increased in the brain during endotoxin-induced systemic inflammation and is localized to numerous cells including astrocytes and microglia — ASN Events
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Strawberry notch homolog 2 gene expression is increased in the brain during endotoxin-induced systemic inflammation and is localized to numerous cells including astrocytes and microglia (#257)

Magdalena Grill 1 2 , Taylor E. Syme 1 , Aline L. Noçon 1 , Iain L. Campbell 1
  1. School of Molecular Bioscience, University of Sydney, Sydney, NSW, Australia
  2. Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria

Aims: In an effort to better understand the function of the cytokine Interleukin (IL)-6 in the murine brain, our group identified the putative DExD/H-box helicase strawberry notch homolog 2 (Sbno2) as a novel IL-6/glycoprotein 130 regulated target gene in murine astrocytes and microglia in vitro. The aim of this study was to determine the regulation and cellular localization of Sbno2 gene expression during neuroinflammatory conditions in vivo.

Methods: Upon endotoxin-induced systemic inflammation (2 mg/kg dual LPS injection, intra-peritoneal, 16 h plus 4 h or 24 h, respectively) in mice, total RNA was isolated from the brain and Sbno2 mRNA levels were determined by RNase protection assay. From a second set of animals, paraformaldehyde-fixed, paraffin-embedded mouse brains were sagitally cut and analysed by in situ hybridization (ISH)/immuno-/histochemistry (IHC).

Results: Sbno2 mRNA levels were highly increased at 4 h and decreased thereafter, but still had elevated levels up to 24 h after the second treatment. In ISH experiments, up-regulated Sbno2 mRNA was mainly co-localized with GFAP-positive astrocytes while lesser numbers of selected tomato lectin-stained microglia and endothelial cells co-localized with Sbno2 mRNA as well.

Conclusions: The results of the current study complement our previous in vitro data and strengthen the notion of a role for Sbno2 in the innate inflammatory response during host-defence.

Supported by NH&MRC grants 632754 and APP1047265 and Austrian Science Fund (FWF): J3081-B09.