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Microglial toll-like receptor 2 contributes to kainic acid-induced glial activation and hippocampal neuronal cell death

Title
Microglial toll-like receptor 2 contributes to kainic acid-induced glial activation and hippocampal neuronal cell death
Authors
Hong J.Cho I.-H.Kwak K.I.Suh E.C.Seo J.Min H.J.Choi S.-Y.Kim C.-H.Park S.H.Jo E.-K.Lee S.Lee K.E.Lee S.J.
Ewha Authors
이경은
SCOPUS Author ID
이경은scopus
Issue Date
2010
Journal Title
Journal of Biological Chemistry
ISSN
0021-9258JCR Link
Citation
vol. 285, no. 50, pp. 39447 - 39457
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Recent studies indicate that Toll-like receptors (TLRs), originally identified as infectious agent receptors, also mediate sterile inflammatory responses during tissue damage. In this study, we investigated the role of TLR2 in excitotoxic hippocampal cell death using TLR2 knock-out (KO) mice. TLR2 expression was up-regulated in microglia in the ipsilateral hippocampus of kainic acid (KA)-injected mice. KA-mediated hippocampal cell death was significantly reduced in TLR2 KO mice compared with wild-type (WT) mice. Similarly, KA-induced glial activation and proinflammatory gene expression in the hippocampus were compromised in TLR2 KO mice. In addition, neurons in organotypic hippocampal slice cultures (OHSCs) from TLR2 KO mouse brains were less susceptible to KA excitotoxicity than WT OHSCs. This protection is partly attributed to decreased expression of proinflammatory genes, such as TNF-α and IL-1β in TLR2 KO mice OHSCs. These data demonstrate conclusively that TLR2 signaling in microglia contributes to KA-mediated innate immune responses and hippocampal excitotoxicity. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
DOI
10.1074/jbc.M110.132522
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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