IL-6 attenuates trimethyltin-induced cognitive dysfunction via activation of JAK2/STAT3, M1 mAChR and ERK signaling network
DC Field | Value | Language |
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dc.contributor.author | Kim, Beom Keun | - |
dc.contributor.author | Haong-Yen Phi Tran | - |
dc.contributor.author | Shin, Eun-Joo | - |
dc.contributor.author | Lee, Chaeyoung | - |
dc.contributor.author | Chung, Yoon Hee | - |
dc.contributor.author | Jeong, Ji Hoon | - |
dc.contributor.author | Bach, Jae-Hyung | - |
dc.contributor.author | Kim, Won-Ki | - |
dc.contributor.author | Park, Dae Hoon | - |
dc.contributor.author | Saito, Kuniaki | - |
dc.contributor.author | Nabeshima, Toshitaka | - |
dc.contributor.author | Kim, Hyoung-Chun | - |
dc.date.available | 2018-05-09T14:07:49Z | - |
dc.date.created | 2018-04-17 | - |
dc.date.issued | 2013-06 | - |
dc.identifier.issn | 0898-6568 | - |
dc.identifier.uri | http://scholarworks.bwise.kr/ssu/handle/2018.sw.ssu/11252 | - |
dc.description.abstract | We previously reported that interleukin (IL)-6 deficiency potentiates trimethyltin (TMT)-induced convulsive neurotoxicity. The purpose in this study was to investigate the molecular mechanism by which cytokines affect TMT-induced cognitive impairment To accomplish this, we examined hippocampal changes in Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling in relation to cholinergic parameters after TMT treatment in mice genetically deficient in IL-6 (IL-6(-/-)), tumor necrosis factor-alpha (TNE-alpha(-/-)), or interferon-gamma (IFN-gamma(-/-)). The IL-6(-/-) mice were the most susceptible to TMT-induced cognitive dysfunction and exhibited significant decreases in JAK2/STAT3 signaling and M1 muscarinic acetylcholine receptor (mAChR) expression, as well as other cholinergic parameters, compared with wild-type (WT) animals. Recombinant IL-6 protein (rIL-6) significantly attenuated these impairments in TMT-treated IL-6(-/-) mice, whereas an IL-6 receptor antibody potentiated these impairments in TMT-treated WT animals. Inhibition of JAK2 with AG490 or inhibition of cholinergic signaling with the M1 mAChR antagonist dicyclomine counteracted the attenuating effects of rIL-6 on phosphotylated extracellular signal-regulated kinase (ERK) expression, or on cognitive impairment in TMT-treated IL-6(-/-) mice. However, neither AG490 nor dicyclomine significantly attenuated effects of rIL-6 on acetylcholinesterase values. Our results suggest that activation of JAK2/STAT3 signaling and upregulation of the M1 mAChR are essential components of IL-6-mediated memory improvement against TMT toxicity. (C) 2013 Elsevier Inc. All rights reserved. | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.relation.isPartOf | CELLULAR SIGNALLING | - |
dc.subject | CENTRAL-NERVOUS-SYSTEM | - |
dc.subject | HIPPOCAMPAL NEUROGENESIS | - |
dc.subject | INDUCED NEUROTOXICITY | - |
dc.subject | LEARNING IMPAIRMENT | - |
dc.subject | RECOGNITION MEMORY | - |
dc.subject | ALZHEIMERS-DISEASE | - |
dc.subject | IN-VIVO | - |
dc.subject | MICE | - |
dc.subject | INTERLEUKIN-6 | - |
dc.subject | RECEPTOR | - |
dc.title | IL-6 attenuates trimethyltin-induced cognitive dysfunction via activation of JAK2/STAT3, M1 mAChR and ERK signaling network | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.cellsig.2013.02.017 | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | CELLULAR SIGNALLING, v.25, no.6, pp.1348 - 1360 | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000319176000002 | - |
dc.identifier.scopusid | 2-s2.0-84876323219 | - |
dc.citation.endPage | 1360 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1348 | - |
dc.citation.title | CELLULAR SIGNALLING | - |
dc.citation.volume | 25 | - |
dc.contributor.affiliatedAuthor | Lee, Chaeyoung | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Cognitive impairments | - |
dc.subject.keywordAuthor | Hippocampus | - |
dc.subject.keywordAuthor | Intedukin-6 gene | - |
dc.subject.keywordAuthor | M1 muscarinic acetylcholine receptor | - |
dc.subject.keywordAuthor | Extracellular signal-regulated kinase | - |
dc.subject.keywordPlus | CENTRAL-NERVOUS-SYSTEM | - |
dc.subject.keywordPlus | HIPPOCAMPAL NEUROGENESIS | - |
dc.subject.keywordPlus | INDUCED NEUROTOXICITY | - |
dc.subject.keywordPlus | LEARNING IMPAIRMENT | - |
dc.subject.keywordPlus | RECOGNITION MEMORY | - |
dc.subject.keywordPlus | ALZHEIMERS-DISEASE | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | INTERLEUKIN-6 | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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