TGF-β induced by interleukin-34-stimulated microglia regulates microglial proliferation and attenuates oligomeric amyloid β neurotoxicity - PubMed (original) (raw)
. 2012 Oct 31;529(1):86-91.
doi: 10.1016/j.neulet.2012.08.071. Epub 2012 Sep 7.
Affiliations
- PMID: 22985514
- DOI: 10.1016/j.neulet.2012.08.071
TGF-β induced by interleukin-34-stimulated microglia regulates microglial proliferation and attenuates oligomeric amyloid β neurotoxicity
Di Ma et al. Neurosci Lett. 2012.
Abstract
Microglia play critical roles in the pathogenesis of Alzheimer's disease (AD). We have previously shown that interleukin-34 (IL-34) enhances microglial proliferation and induces microglial neuroprotective properties against oligomeric amyloid β (oAβ) toxicity by producing insulin degrading enzyme, an Aβ degrading enzyme, and anti-oxidant enzyme heme oxygenase-1. In this study, we found that IL-34 dose-dependently induces TGF-β in microglia, and that TGF-β attenuates oAβ neurotoxicity in neuron microglial co-cultures. The TGF-β 1 receptor kinase inhibitor SD208 enhances microglial proliferation by IL-34 and suppresses the neuroprotective effect of IL-34-treated microglia. These findings suggest that TGF-β produced by IL-34-treated microglia is a negative regulator of microglial proliferation and enhances the neuroprotective property of microglia.
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
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