Journal
NEUROSCIENCE LETTERS
Volume 529, Issue 1, Pages 86-91Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2012.08.071
Keywords
TGF-beta; IL-34; Microglia; Neuroprotection; Oligomeric amyloid beta
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Funding
- China Scholarship Council (CSC)
- Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT)
- MEXT
- Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO)
- Grants-in-Aid for Scientific Research [24659430] Funding Source: KAKEN
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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 beta (oA beta) toxicity by producing insulin degrading enzyme, an A beta degrading enzyme, and anti-oxidant enzyme heme oxygenase-1. In this study, we found that IL-34 dose-dependently induces TGF-beta in microglia, and that TGF-beta attenuates oA beta neurotoxicity in neuron microglial co-cultures. The TGF-beta 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-beta produced by IL-34-treated microglia is a negative regulator of microglial proliferation and enhances the neuroprotective property of microglia. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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