Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 정영해 | - |
dc.date.accessioned | 2016-08-28T10:08:30Z | - |
dc.date.available | 2016-08-28T10:08:30Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 0014-4886 | - |
dc.identifier.other | OAK-9023 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/222850 | - |
dc.description.abstract | Evidence indicates that norepinephrine (NE) has antiinflammatory activities and plays a neuroprotective role where inflammatory events contribute to Alzheimer's disease pathology. Here, we evaluated the effects of NE on amyloid beta 1-42 (Aβ1-42)-induced cytotoxicity and proinflammatory cytokine/chemokine secretion, and determined the mechanisms through which NE exerts its actions in human THP-1 macrophages. NE clearly reduced the Aβ1-42-mediated production of the proinflammatory chemokine, monocytic chemotactic protein-1 (MCP-1/CCL2). In contrast to its ability to reduce MCP-1 secretion, NE enhanced the amounts of the proinflammatory cytokine interleukin (IL)-1β secreted from Aβ1-42 treated cells. NE significantly reduced the Aβ1-42-induced cytotoxicity in situations where it contributed to the increased IL-1β and decreased MCP-1 during Aβ1-42 stimulation. The ability of NE to differentially modulate the Aβ1-42-induced immune responses was mediated by β-adrenoceptors, as the aforementioned effects were replicated by the β-adrenoceptor agonist, isoproterenol, and blocked by the β-adrenoceptor antagonist, dl-propranolol. Of note, the NE effects on Aβ1-42-induced responses were mimicked by dbcAMP and forskolin, but significantly blocked by H89, an inhibitor of PKA. Moreover, NE abolished Aβ1-42-mediated decline of CREB phosphorylation. Overall, NE suppresses Aβ1-42-mediated cytotoxicity and MCP-1 secretion, but enhances Aβ-mediated IL-1β secretion through action at β-adrenoceptors, accompanied by activation of cAMP/PKA pathway and CREB in human microglia-like THP-1 cells. © 2012 Elsevier Inc.. | - |
dc.language | English | - |
dc.title | Norepinephrine differentially modulates the innate inflammatory response provoked by amyloid-β peptide via action at β-adrenoceptors and activation of cAMP/PKA pathway in human THP-1 macrophages | - |
dc.type | Article | - |
dc.relation.issue | 2 | - |
dc.relation.volume | 236 | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 199 | - |
dc.relation.lastpage | 206 | - |
dc.relation.journaltitle | Experimental Neurology | - |
dc.identifier.doi | 10.1016/j.expneurol.2012.05.008 | - |
dc.identifier.wosid | WOS:000306622900001 | - |
dc.identifier.scopusid | 2-s2.0-84861734808 | - |
dc.author.google | Yang J.H. | - |
dc.author.google | Lee E.O. | - |
dc.author.google | Kim S.E. | - |
dc.author.google | Suh Y.-H. | - |
dc.author.google | Chong Y.H. | - |
dc.contributor.scopusid | 정영해(7201371824) | - |
dc.date.modifydate | 20180901081003 | - |