Please use this identifier to cite or link to this item:
http://hdl.handle.net/10397/93659
DC Field | Value | Language |
---|---|---|
dc.contributor | Department of Health Technology and Informatics | en_US |
dc.creator | Cai, Y | en_US |
dc.creator | Zhang, Y | en_US |
dc.creator | Chen, H | en_US |
dc.creator | Sun, XH | en_US |
dc.creator | Zhang, P | en_US |
dc.creator | Zhang, L | en_US |
dc.creator | Liao, MY | en_US |
dc.creator | Zhang, F | en_US |
dc.creator | Xia, ZY | en_US |
dc.creator | Man, RYK | en_US |
dc.creator | Feinberg, MW | en_US |
dc.creator | Leung, SWS | en_US |
dc.date.accessioned | 2022-07-20T02:27:35Z | - |
dc.date.available | 2022-07-20T02:27:35Z | - |
dc.identifier.uri | http://hdl.handle.net/10397/93659 | - |
dc.language.iso | en | en_US |
dc.publisher | Nature Publishing Group | en_US |
dc.rights | © The Author(s), under exclusive licence to CPS and SIMM 2021 | en_US |
dc.rights | This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use (https://www.springernature.com/gp/open-research/policies/accepted-manuscript-terms), but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1038/s41401-021-00611-w. | en_US |
dc.subject | Endothelial cells | en_US |
dc.subject | Inflammation | en_US |
dc.subject | MiR-17-3p | en_US |
dc.subject | NIK and IKKβ binding protein | en_US |
dc.subject | Nuclear factor kappa B | en_US |
dc.title | MicroRNA-17-3p suppresses NF-κB-mediated endothelial inflammation by targeting NIK and IKKβ binding protein | en_US |
dc.type | Journal/Magazine Article | en_US |
dc.identifier.spage | 2046 | en_US |
dc.identifier.epage | 2057 | en_US |
dc.identifier.volume | 42 | en_US |
dc.identifier.issue | 12 | en_US |
dc.identifier.doi | 10.1038/s41401-021-00611-w | en_US |
dcterms.abstract | Nuclear factor kappa B (NF-κB) activation contributes to many vascular inflammatory diseases. The present study tested the hypothesis that microRNA-17-3p (miR-17-3p) suppresses the pro-inflammatory responses via NF-κB signaling in vascular endothelium. Human umbilical vein endothelial cells (HUVECs), transfected with or without miR-17-3p agomir/antagomir, were exposed to lipopolysaccharide (LPS), and the inflammatory responses were determined. The cellular target of miR-17-3p was examined with dual-luciferase reporter assay. Mice were treated with miR-17-3p agomir and the degree of LPS-induced inflammation was determined. In HUVECs, LPS caused upregulation of miR-17-3p. Overexpression of miR-17-3p in HUVECs inhibited NIK and IKKβ binding protein (NIBP) protein expression and suppressed LPS-induced phosphorylation of inhibitor of kappa Bα (IκBα) and NF-κB-p65. The reduced NF-κB activity was paralleled by decreased protein levels of NF-κB-target gene products including pro-inflammatory cytokine [interleukin 6], chemokines [interleukin 8 and monocyte chemoattractant protein-1] and adhesion molecules [vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and E-selectin]. Immunostaining revealed that overexpression of miR-17-3p reduced monocyte adhesion to LPS-stimulated endothelial cells. Inhibition of miR-17-3p with antagomir has the opposite effect on LPS-induced inflammatory responses in HUVECs. The anti-inflammatory effect of miR-17-3p was mimicked by NIBP knockdown. In mice treated with LPS, miR-17-3p expression was significantly increased. Systemic administration of miR-17-3p for 3 days suppressed LPS-induced NF-κB activation and monocyte adhesion to endothelium in lung tissues of the mice. In conclusion, miR-17-3p inhibits LPS-induced NF-κB activation in HUVECs by targeting NIBP. The findings therefore suggest that miR-17-3p is a potential therapeutic target/agent in the management of vascular inflammatory diseases. | en_US |
dcterms.accessRights | open access | en_US |
dcterms.bibliographicCitation | Acta pharmacologica sinica, Dec. 2021, v. 42, no. 12, p. 2046-2057 | en_US |
dcterms.isPartOf | Acta pharmacologica sinica | en_US |
dcterms.issued | 2021-12 | - |
dc.identifier.scopus | 2-s2.0-85101321124 | - |
dc.identifier.pmid | 33623121 | - |
dc.identifier.eissn | 1671-4083 | en_US |
dc.description.validate | 202207 bcww | en_US |
dc.description.oa | Accepted Manuscript | en_US |
dc.identifier.FolderNumber | HTI-0026 | - |
dc.description.fundingSource | Others | en_US |
dc.description.fundingText | Health and Medical Research Fund; Seed Fund for Basic Research of the University of Hong Kong; National Institutes of Health; Arthur K. Watson Charitable Trust; Dr. Ralph & Marian Falk Medical Research Trust | en_US |
dc.description.pubStatus | Published | en_US |
dc.identifier.OPUS | 46182275 | - |
Appears in Collections: | Journal/Magazine Article |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
Cai_MicroRNA-17-3p_Suppresses_Inflammation.pdf | Pre-Published version | 1.29 MB | Adobe PDF | View/Open |
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