Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/45550
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dc.contributor.authorMa, Xin-
dc.contributor.authorWang, Teng-
dc.contributor.authorZhao, Zhen-Long-
dc.contributor.authorJiang, Yu-
dc.contributor.authorYe, Shu-
dc.date.accessioned2019-09-10T15:10:39Z-
dc.date.available2019-09-10T15:10:39Z-
dc.date.issued2018-12-17-
dc.identifier.citationMediators of Inflammation, 2018, Volume 2018, Article ID 8907143, 9 pagesen
dc.identifier.urihttps://www.hindawi.com/journals/mi/2018/8907143/en
dc.identifier.urihttp://hdl.handle.net/2381/45550-
dc.descriptionSupplementary 1. Fig. S1: hierarchical clustering for the levels of ABCA1 and lncRNA with or without 50 μM propofol. Hierarchical clustering based on the selected set [393 mRNAs (ABCA1 included) and 265 lncRNAs (LOC286367 included)] (red: upregulation; green: downregulation; black: no significant change). Supplementary 2. Figure S2: diagram about the genomic locations and opposite transcriptional directions of LOC286367 and ABCA1.en
dc.description.abstractWe previously reported that propofol upregulated the expression of ATP-binding cassette transporter subfamily A member 1 (ABCA1) via peroxisome proliferator-activated receptor gamma/liver X receptor in macrophage-derived foam cells. Here, we provide evidence that in addition to inducing ABCA1 expression, propofol represses proinflammatory cytokine production by increasing ABCA1 expression in a LOC286367-dependent manner. Western blot analysis showed that ABCA1 expression was elevated in macrophages by propofol treatment and this effect was markedly reduced by LOC286367 overexpression. Moreover, propofol treatment downregulated the production of the proinflammatory cytokines interleukin-6, tumor necrosis factor, and interferon gamma in lipopolysaccharide-stimulated macrophages by enhancing ABCA1 expression. Notably, propofol achieved this effect in a LOC286367-dependent manner. To the best of our knowledge, this is the first report of the mechanism in which propofol represses proinflammatory cytokine production mediated by ABCA1.en
dc.description.sponsorshipThis work was supported by the National Natural Science Foundation of China (grant no. 81500387) and the President Foundation of Nanfang Hospital, Southern Medical University (2016B002). SY thanks the support of the British Heart Foundation (grant nos. RG/16/13/32609 and PG/16/9/31995) and the National Natural Science Foundation of China (grant no. 81370202). This work falls under the portfolio of research conducted within the NIHR Leicester Biomedical Research Centre.en
dc.language.isoenen
dc.publisherHindawien
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/30647536-
dc.rightsCopyright © the authors, 2018. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en
dc.titlePropofol Suppresses Proinflammatory Cytokine Production by Increasing ABCA1 Expression via Mediation by the Long Noncoding RNA LOC286367.en
dc.typeJournal Articleen
dc.identifier.doi10.1155/2018/8907143-
dc.identifier.eissn1466-1861-
dc.description.statusPeer-revieweden
dc.description.versionPublisher Versionen
dc.type.subtypeJournal Article-
pubs.organisational-group/Organisationen
pubs.organisational-group/Organisation/COLLEGE OF LIFE SCIENCESen
pubs.organisational-group/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicineen
pubs.organisational-group/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicine/Department of Cardiovascular Sciencesen
dc.dateaccepted2018-10-14-
Appears in Collections:Published Articles, Dept. of Cardiovascular Sciences



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