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Conference Paper: MicroRNA-17-3p blunts endothelial responses to inflammatory stimuli
Title | MicroRNA-17-3p blunts endothelial responses to inflammatory stimuli |
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Authors | |
Issue Date | 2019 |
Citation | 13th International Symposium on Mechanisms of VasoDilatation & 7th International Symposium on Endothelium-Dependent Hyperpolarization (MOVD/EDH 2019), Rotterdam, The Netherlands, 20–22 May 2019 How to Cite? |
Abstract | Introduction: Micro-ribonucleic acids (miRNAs) are small endogenous non-coding RNAs which play an important role in vascular inflammation. Previous studies demonstrate that miRNA-17-3p reduces inflammatory responses of human endothelial cells to the bacterial endotoxin lipopolysaccharide (LPS). Vascular inflammation is a risk factor for cardiovascular diseases, and is associated with endothelial dysfunction.
Aims: To determine whether or not miRNA-17-3p protects against impairment of endothelial function during inflammation, and, if so, whether or not its anti-inflammatory effect is selective for LPS.
Methods: Human aortic and umbilical vein endothelial cells, without or with transfection with miRNA-17-3p agomir (synthetic RNA duplexes stimulating miRNA-17-3p activity) or its negative control, were exposed to the inflammatory stimuli LPS or human immunodeficiency virus (HIV) proteins gp-120. After treatment, the level of miRNA-17-3p was assessed with quantitative reverse transcription-polymerase chain reaction. The levels of inflammatory mediators [interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1)], and the protein levels of endothelial nitric oxide synthase (eNOS) and cyclooxygenases (COXs), enzymes responsible for the generation of endothelium-derived
nitric oxide and vasoactive prostanoids, were measured with enzyme immunoassays and Western immunoblotting, respectively.
Results: In human endothelial cells treated with LPS or gp-120, the amounts of IL-6 and MCP-1, and the protein levels of COX-1 were increased. LPS increased the expression level of miRNA-17-3p; this upregulation was paralleled by reduced levels of the inflammatory mediators induced by LPS. In endothelial cells transfected with miRNA-17-3p agomir, the protein level of eNOS was augmented while that of COX-2 was reduced.
Conclusion: These findings suggest that miRNA-17-3p reduces the inflammatory responses of endothelial cells to different inflammatory stimuli, LPS and HIV proteins. Upregulation of miRNA-17-3p may enhance endothelial function in terms of regulation of vascular tone, as demonstrated by the increased eNOS (favoring the production of NO) level and the reduced COX-2 presence (blunting the release of vasoconstrictor prostanoids). |
Description | Poster Session I - no. P09 |
Persistent Identifier | http://hdl.handle.net/10722/279544 |
DC Field | Value | Language |
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dc.contributor.author | Ren, W | - |
dc.contributor.author | Cai, Y | - |
dc.contributor.author | Zhang, Y | - |
dc.contributor.author | Ho, EYW | - |
dc.contributor.author | Lam, JKW | - |
dc.contributor.author | Vanhoutte, PMGR | - |
dc.contributor.author | Leung, SWS | - |
dc.date.accessioned | 2019-11-01T07:19:23Z | - |
dc.date.available | 2019-11-01T07:19:23Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | 13th International Symposium on Mechanisms of VasoDilatation & 7th International Symposium on Endothelium-Dependent Hyperpolarization (MOVD/EDH 2019), Rotterdam, The Netherlands, 20–22 May 2019 | - |
dc.identifier.uri | http://hdl.handle.net/10722/279544 | - |
dc.description | Poster Session I - no. P09 | - |
dc.description.abstract | Introduction: Micro-ribonucleic acids (miRNAs) are small endogenous non-coding RNAs which play an important role in vascular inflammation. Previous studies demonstrate that miRNA-17-3p reduces inflammatory responses of human endothelial cells to the bacterial endotoxin lipopolysaccharide (LPS). Vascular inflammation is a risk factor for cardiovascular diseases, and is associated with endothelial dysfunction. Aims: To determine whether or not miRNA-17-3p protects against impairment of endothelial function during inflammation, and, if so, whether or not its anti-inflammatory effect is selective for LPS. Methods: Human aortic and umbilical vein endothelial cells, without or with transfection with miRNA-17-3p agomir (synthetic RNA duplexes stimulating miRNA-17-3p activity) or its negative control, were exposed to the inflammatory stimuli LPS or human immunodeficiency virus (HIV) proteins gp-120. After treatment, the level of miRNA-17-3p was assessed with quantitative reverse transcription-polymerase chain reaction. The levels of inflammatory mediators [interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1)], and the protein levels of endothelial nitric oxide synthase (eNOS) and cyclooxygenases (COXs), enzymes responsible for the generation of endothelium-derived nitric oxide and vasoactive prostanoids, were measured with enzyme immunoassays and Western immunoblotting, respectively. Results: In human endothelial cells treated with LPS or gp-120, the amounts of IL-6 and MCP-1, and the protein levels of COX-1 were increased. LPS increased the expression level of miRNA-17-3p; this upregulation was paralleled by reduced levels of the inflammatory mediators induced by LPS. In endothelial cells transfected with miRNA-17-3p agomir, the protein level of eNOS was augmented while that of COX-2 was reduced. Conclusion: These findings suggest that miRNA-17-3p reduces the inflammatory responses of endothelial cells to different inflammatory stimuli, LPS and HIV proteins. Upregulation of miRNA-17-3p may enhance endothelial function in terms of regulation of vascular tone, as demonstrated by the increased eNOS (favoring the production of NO) level and the reduced COX-2 presence (blunting the release of vasoconstrictor prostanoids). | - |
dc.language | eng | - |
dc.relation.ispartof | 13th International Symposium on Mechanisms of Vasodilatation and 7th International Symposium on Endothelium-Dependent Hyperpolarization (MOVD/EDH 2019) | - |
dc.title | MicroRNA-17-3p blunts endothelial responses to inflammatory stimuli | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Cai, Y: caidavid@hku.hk | - |
dc.identifier.email | Ho, EYW: yeewaho@hkucc.hku.hk | - |
dc.identifier.email | Lam, JKW: jkwlam@hku.hk | - |
dc.identifier.email | Vanhoutte, PMGR: vanhoutt@hku.hk | - |
dc.identifier.email | Leung, SWS: swsleung@hku.hk | - |
dc.identifier.authority | Lam, JKW=rp01346 | - |
dc.identifier.authority | Vanhoutte, PMGR=rp00238 | - |
dc.identifier.authority | Leung, SWS=rp00235 | - |
dc.identifier.hkuros | 308350 | - |