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Microglial Toll-like Receptor 2 Contributes to Kainic Acid-induced Glial Activation and Hippocampal Neuronal Cell Death

Cited 43 time in Web of Science Cited 44 time in Scopus
Authors
Hong, Jinpyo; Cho, Ik-Hyun; Kwak, Kyung Il; Suh, Eun Cheng; Min, Hyun Jung; Kim, Chong-Hyun; Jo, Eun-Kyeong; Lee, Kyung Eun; Lee, Sung Joong; Lee, Soojin; Park, Seung Hwa; Choi, Se-Young; Seo, Jinsoo
Issue Date
2010-12
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, Vol.285, No.50, pp.39447-39457
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-alpha and IL-1 beta in TLR2 KO mice OHSCs. These data demonstrate conclusively that TLR2 signaling in microglia contributes to KA-mediated innate immune responses and hippocampal excitotoxicity.
ISSN
0021-9258
Language
English
URI
http://hdl.handle.net/10371/80391
DOI
https://doi.org/10.1074/jbc.M110.132522
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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