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Primary cilia modulate TLR4-mediated inflammatory responses in hippocampal neurons

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dc.contributor.authorBaek, Hyunjung
dc.contributor.authorShin, Hyo Jung
dc.contributor.authorKim, Jwa-Jin
dc.contributor.authorShin, Nara
dc.contributor.authorKim, Sena
dc.contributor.authorYi, Min-Hee
dc.contributor.authorZhang, Enji
dc.contributor.authorHong, Jinpyo
dc.contributor.authorKang, Joon Won
dc.contributor.authorKim, Yonghyun
dc.contributor.authorKim, Cuk-Seong
dc.contributor.authorKim, Dong Woon
dc.contributor.otherChungnam National University
dc.contributor.otherChungnam National University Hospital
dc.contributor.otherUniversity of Texas Medical Branch Galveston
dc.contributor.otherYanbian University
dc.contributor.otherUniversity of Alabama Tuscaloosa
dc.date.accessioned2023-10-02T15:17:14Z
dc.date.available2023-10-02T15:17:14Z
dc.date.issued2017
dc.description.abstractBackground: The primary cilium is an organelle that can act as a master regulator of cellular signaling. Despite the presence of primary cilia in hippocampal neurons, their function is not fully understood. Recent studies have demonstrated that the primary cilium influences interleukin (IL)-1 beta-induced NF-kappa B signaling, ultimately mediating the inflammatory response. We, therefore, investigated ciliary function and NF-kappa B signaling in lipopolysaccharide (LPS)-induced neuroinflammation in conjunction with ciliary length analysis. Methods: Since TLR4/NF-kappa B signaling is a well-known inflammatory pathway, we measured ciliary length and inflammatory mediators in wild type (WT) and TLR4(-/-) mice injected with LPS. Next, to exclude the effects of microglial TLR4, we examined the ciliary length, ciliary components, inflammatory cytokine, and mediators in HT22 hippocampal neuronal cells. Results: Primary ciliary length decreased in hippocampal pyramidal neurons after intracerebroventricular injection of LPS in WT mice, whereas it increased in TLR4(-/-) mice. LPS treatment decreased primary ciliary length, activated NF-kappa B signaling, and increased Cox2 and iNOS levels in HT22 hippocampal neurons. In contrast, silencing Kif3a, a key protein component of cilia, increased ARL13B ciliary protein levels and suppressed NF-kappa B signaling and expression of inflammatory mediators. Conclusions: These data suggest that LPS-induced NF-kappa B signaling and inflammatory mediator expression are modulated by cilia and that the blockade of primary cilium formation by Kif3a siRNA regulates TLR4-induced NF-kappa B signaling. We propose that primary cilia are critical for regulating NF-kappa B signaling events in neuroinflammation and in the innate immune response.en_US
dc.format.mediumelectronic
dc.format.mimetypeapplication/pdf
dc.identifier.citationBaek, H., Shin, H. J., Kim, J.-J., Shin, N., Kim, S., Yi, M.-H., Zhang, E., Hong, J., Kang, J. W., Kim, Y., Kim, C.-S., & Kim, D. W. (2017). Primary cilia modulate TLR4-mediated inflammatory responses in hippocampal neurons. In Journal of Neuroinflammation (Vol. 14, Issue 1). Springer Science and Business Media LLC. https://doi.org/10.1186/s12974-017-0958-7
dc.identifier.doi10.1186/s12974-017-0958-7
dc.identifier.orcidhttps://orcid.org/0000-0001-7691-1394
dc.identifier.orcidhttps://orcid.org/0000-0001-6344-1258
dc.identifier.orcidhttps://orcid.org/0000-0001-5756-3814
dc.identifier.orcidhttps://orcid.org/0000-0001-7647-6089
dc.identifier.urihttps://ir.ua.edu/handle/123456789/12584
dc.languageEnglish
dc.language.isoen_US
dc.publisherBiomed Central
dc.rights.licenseAttribution 4.0 International (CC BY 4.0)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectPrimary cilia
dc.subjectHippocampus
dc.subjectNF kappa b
dc.subjectTLR4
dc.subjectNeuroinflammation
dc.subjectCHOLINERGIC ANTIINFLAMMATORY PATHWAY
dc.subjectEPITHELIAL-CELLS
dc.subjectNITRIC-OXIDE
dc.subjectLIPOPOLYSACCHARIDE
dc.subjectDISEASE
dc.subjectEXPRESSION
dc.subjectINDUCTION
dc.subjectBRAIN
dc.subjectNEUROGENESIS
dc.subjectCILIOGENESIS
dc.subjectImmunology
dc.subjectNeurosciences
dc.titlePrimary cilia modulate TLR4-mediated inflammatory responses in hippocampal neuronsen_US
dc.typeArticle
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