Wnt3a induces exosome secretion from primary cultured rat microglia

84Citations
Citations of this article
126Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Background: Microglia, the immune effector cells of the CNS and the signaling molecule Wnt, both play critical roles in neurodevelopment and neurological disease. Here we describe the inducible release of exosomes from primary cultured rat microglia following treatment with recombinant carrier-free Wnt3a.Results: Wnt3a was internalised into microglia, being detectable in early endosomes, and secreted in exosomes through a GSK3-independent mechanism. Electron microscopy demonstrated that exosomes were elliptical, electron-dense (100 nm) vesicles that coalesced with time in vitro. In contrast to microglia, primary cortical neurons released exosomes constitutively and the quantity of exosomes released was not altered by Wnt3a treatment. The proteomic profile of the microglial-derived exosomes was characterised using liquid chromatography-tandem mass spectrometry (LC/MS/MS) and the vesicles were found to be associated with proteins involved in cellular architecture, metabolism, protein synthesis and protein degradation including β-actin, glyceraldehyde-3-phosphate dehydrogenase, ribosomal subunits and ubiquitin (45 proteins in total). Unlike lipopolysaccharide, Wnt3a did not induce a neurotoxic, pro-inflammatory phenotype in primary microglia.Conclusion: These findings reveal a novel mechanism through which Wnt3a signals in microglia resulting in the release of exosomes loaded with proteinaceous cargo. © 2012 Hooper et al.; licensee BioMed Central Ltd.

Cite

CITATION STYLE

APA

Hooper, C., Sainz-Fuertes, R., Lynham, S., Hye, A., Killick, R., Warley, A., … Lovestone, S. (2012). Wnt3a induces exosome secretion from primary cultured rat microglia. BMC Neuroscience, 13(1). https://doi.org/10.1186/1471-2202-13-144

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free