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Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

Title
Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States
Authors
Woller S.A.Choi S.-H.An E.J.Low H.Schneider D.A.Ramachandran R.Kim J.Bae Y.S.Sviridov D.Corr M.Yaksh T.L.Miller Y.I.
Ewha Authors
배윤수
SCOPUS Author ID
배윤수scopus
Issue Date
2018
Journal Title
Cell Reports
ISSN
2211-1247JCR Link
Citation
Cell Reports vol. 23, no. 9, pp. 2667 - 2677
Keywords
AIBPallodyniachemotherapycholesterolchronic paininflammationlipid raftsneuroinflammationneuropathic painTLR4
Publisher
Elsevier B.V.
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Apolipoprotein A-I binding protein (AIBP) reduces lipid raft abundance by augmenting the removal of excess cholesterol from the plasma membrane. Here, we report that AIBP prevents and reverses processes associated with neuroinflammatory-mediated spinal nociceptive processing. The mechanism involves AIBP binding to Toll-like receptor-4 (TLR4) and increased binding of AIBP to activated microglia, which mediates selective regulation of lipid rafts in inflammatory cells. AIBP-mediated lipid raft reductions downregulate LPS-induced TLR4 dimerization, inflammatory signaling, and expression of cytokines in microglia. In mice, intrathecal injections of AIBP reduce spinal myeloid cell lipid rafts, TLR4 dimerization, neuroinflammation, and glial activation. Intrathecal AIBP reverses established allodynia in mice in which pain states were induced by the chemotherapeutic cisplatin, intraplantar formalin, or intrathecal LPS, all of which are pro-nociceptive interventions known to be regulated by TLR4 signaling. These findings demonstrate a mechanism by which AIBP regulates neuroinflammation and suggest the therapeutic potential of AIBP in treating preexisting pain states. Woller et al. report that ApoA-I binding protein (AIBP) selectively regulates, via TLR4 binding, cholesterol removal and normalization of lipid rafts in inflamed microglia. Spinal delivery of AIBP reduces neuroinflammation and prevents and reverses neuropathic pain states, such as chemotherapy-induced peripheral neuropathy, with an effect sustained for >2 months. © 2018 The Author(s)
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DOI
10.1016/j.celrep.2018.04.110
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자연과학대학 > 생명과학전공 > Journal papers
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