Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells
We investigated the role of NADPH oxidase 4 (Nox4) on lipopolysaccharide (LPS)-induced proinflammatory responses by human aortic endothelial cells (HAECs). Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (a...
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| Veröffentlicht in: | Cardiovascular research 2006-12, Vol.72 (3), p.447-455 |
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| creator | HYE SUN PARK JUNG NYEO CHUN HYE YOUNG JUNG CHOI, Chulhee YUN SOO BAE |
| description | We investigated the role of NADPH oxidase 4 (Nox4) on lipopolysaccharide (LPS)-induced proinflammatory responses by human aortic endothelial cells (HAECs).
Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (amino acids 739-769) is the responsible domain for interaction with the COOH terminal of Nox4 (amino acids 451-530). Consistently, overexpression of the COOH-terminal region of Nox4 inhibited nuclear factor-kappaB activation in response to LPS. Downregulation of Nox4 by transfection of siRNA specific to Nox4 in HAECs resulted in a failure to induce reactive oxygen species (ROS) generation and subsequent expression of intercellular adhesion molecule-1 (ICAM-1) and chemokines such as IL-8 and monocyte chemoattractant protein-1 (MCP-1) in response to LPS. Furthermore, transient transfection of endothelial cells with Nox4 siRNA led to a decrease in migration and adhesion of monocytes in response to LPS by 36% and 52%, respectively.
Nox4 plays a central role in LPS-induced proinflammatory responses by endothelial cells in an ROS-dependent manner. |
| doi_str_mv | 10.1016/j.cardiores.2006.09.012 |
| format | Article |
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Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (amino acids 739-769) is the responsible domain for interaction with the COOH terminal of Nox4 (amino acids 451-530). Consistently, overexpression of the COOH-terminal region of Nox4 inhibited nuclear factor-kappaB activation in response to LPS. Downregulation of Nox4 by transfection of siRNA specific to Nox4 in HAECs resulted in a failure to induce reactive oxygen species (ROS) generation and subsequent expression of intercellular adhesion molecule-1 (ICAM-1) and chemokines such as IL-8 and monocyte chemoattractant protein-1 (MCP-1) in response to LPS. Furthermore, transient transfection of endothelial cells with Nox4 siRNA led to a decrease in migration and adhesion of monocytes in response to LPS by 36% and 52%, respectively.
Nox4 plays a central role in LPS-induced proinflammatory responses by endothelial cells in an ROS-dependent manner.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/j.cardiores.2006.09.012</identifier><identifier>PMID: 17064675</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Aorta ; Atherosclerosis (general aspects, experimental research) ; Bacterial Infections - enzymology ; Bacterial Infections - immunology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cell Adhesion - drug effects ; Cell Movement - drug effects ; Cell Nucleus - metabolism ; Cells, Cultured ; Chemokine CCL2 - analysis ; Endothelial Cells - enzymology ; Endothelial Cells - immunology ; Humans ; Hydrogen Peroxide - analysis ; Intercellular Adhesion Molecule-1 - analysis ; Interleukin-8 - analysis ; Lipopolysaccharides - pharmacology ; Medical sciences ; Monocytes - drug effects ; NADPH Oxidase 4 ; NADPH Oxidases - genetics ; NADPH Oxidases - physiology ; NF-kappa B - metabolism ; Protein Binding ; Reverse Transcriptase Polymerase Chain Reaction ; RNA Interference ; RNA, Small Interfering - pharmacology ; Transfection - methods ; Two-Hybrid System Techniques</subject><ispartof>Cardiovascular research, 2006-12, Vol.72 (3), p.447-455</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-6b943481604e9b0569f461d1dc195b73ab50351300314833104bc2afdafdf4803</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18287930$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17064675$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HYE SUN PARK</creatorcontrib><creatorcontrib>JUNG NYEO CHUN</creatorcontrib><creatorcontrib>HYE YOUNG JUNG</creatorcontrib><creatorcontrib>CHOI, Chulhee</creatorcontrib><creatorcontrib>YUN SOO BAE</creatorcontrib><title>Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>We investigated the role of NADPH oxidase 4 (Nox4) on lipopolysaccharide (LPS)-induced proinflammatory responses by human aortic endothelial cells (HAECs).
Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (amino acids 739-769) is the responsible domain for interaction with the COOH terminal of Nox4 (amino acids 451-530). Consistently, overexpression of the COOH-terminal region of Nox4 inhibited nuclear factor-kappaB activation in response to LPS. Downregulation of Nox4 by transfection of siRNA specific to Nox4 in HAECs resulted in a failure to induce reactive oxygen species (ROS) generation and subsequent expression of intercellular adhesion molecule-1 (ICAM-1) and chemokines such as IL-8 and monocyte chemoattractant protein-1 (MCP-1) in response to LPS. Furthermore, transient transfection of endothelial cells with Nox4 siRNA led to a decrease in migration and adhesion of monocytes in response to LPS by 36% and 52%, respectively.
Nox4 plays a central role in LPS-induced proinflammatory responses by endothelial cells in an ROS-dependent manner.</description><subject>Aorta</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Bacterial Infections - enzymology</subject><subject>Bacterial Infections - immunology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cell Nucleus - metabolism</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - analysis</subject><subject>Endothelial Cells - enzymology</subject><subject>Endothelial Cells - immunology</subject><subject>Humans</subject><subject>Hydrogen Peroxide - analysis</subject><subject>Intercellular Adhesion Molecule-1 - analysis</subject><subject>Interleukin-8 - analysis</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Medical sciences</subject><subject>Monocytes - drug effects</subject><subject>NADPH Oxidase 4</subject><subject>NADPH Oxidases - genetics</subject><subject>NADPH Oxidases - physiology</subject><subject>NF-kappa B - metabolism</subject><subject>Protein Binding</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Transfection - methods</subject><subject>Two-Hybrid System Techniques</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN1q3DAQRkVoSLZJXqHVTXNnZ8b6sX0Z0qYphDaE5FrIksxqkS1HsqH79vWSpYGBYeDMzMch5CtCiYDyZlcanayPyeWyApAltCVgdUI2WAtRsIqLT2QDAE0hmWTn5HPOu3UUouZn5BxrkFzWYkPenmNwNPb09-33pwca_3qrs6Oc-pEGP8Uphn3Wxmx18tYVfrSLcZZOKfqxD3oY9BzTnq45pjhml2m3p9tl0CPVMc3eUDfaOG9d8DpQ40LIl-S01yG7q2O_IK_3P17uHorHPz9_3d0-FoYLOReyaznjDUrgru1AyLbnEi1ag63oaqY7AUwgA2DIG8YQeGcq3du1et4AuyDX73fXrG-Ly7MafD4k0KOLS1ayQURZHcD6HTQp5pxcr6bkB532CkEdbKud-m9bHWwraNVqe938cnyxdIOzH3tHvSvw7QjobHTokx6Nzx9cUzV1y4D9A0W2jDY</recordid><startdate>20061201</startdate><enddate>20061201</enddate><creator>HYE SUN PARK</creator><creator>JUNG NYEO CHUN</creator><creator>HYE YOUNG JUNG</creator><creator>CHOI, Chulhee</creator><creator>YUN SOO BAE</creator><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20061201</creationdate><title>Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells</title><author>HYE SUN PARK ; JUNG NYEO CHUN ; HYE YOUNG JUNG ; CHOI, Chulhee ; YUN SOO BAE</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-6b943481604e9b0569f461d1dc195b73ab50351300314833104bc2afdafdf4803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Aorta</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Bacterial Infections - enzymology</topic><topic>Bacterial Infections - immunology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cell Nucleus - metabolism</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - analysis</topic><topic>Endothelial Cells - enzymology</topic><topic>Endothelial Cells - immunology</topic><topic>Humans</topic><topic>Hydrogen Peroxide - analysis</topic><topic>Intercellular Adhesion Molecule-1 - analysis</topic><topic>Interleukin-8 - analysis</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Medical sciences</topic><topic>Monocytes - drug effects</topic><topic>NADPH Oxidase 4</topic><topic>NADPH Oxidases - genetics</topic><topic>NADPH Oxidases - physiology</topic><topic>NF-kappa B - metabolism</topic><topic>Protein Binding</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Transfection - methods</topic><topic>Two-Hybrid System Techniques</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HYE SUN PARK</creatorcontrib><creatorcontrib>JUNG NYEO CHUN</creatorcontrib><creatorcontrib>HYE YOUNG JUNG</creatorcontrib><creatorcontrib>CHOI, Chulhee</creatorcontrib><creatorcontrib>YUN SOO BAE</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HYE SUN PARK</au><au>JUNG NYEO CHUN</au><au>HYE YOUNG JUNG</au><au>CHOI, Chulhee</au><au>YUN SOO BAE</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2006-12-01</date><risdate>2006</risdate><volume>72</volume><issue>3</issue><spage>447</spage><epage>455</epage><pages>447-455</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>We investigated the role of NADPH oxidase 4 (Nox4) on lipopolysaccharide (LPS)-induced proinflammatory responses by human aortic endothelial cells (HAECs).
Yeast two-hybrid and glutathione-S-transferase pull-down assays indicated that the cytosolic Toll/IL-1R region of Toll-like receptor 4 (TLR4) (amino acids 739-769) is the responsible domain for interaction with the COOH terminal of Nox4 (amino acids 451-530). Consistently, overexpression of the COOH-terminal region of Nox4 inhibited nuclear factor-kappaB activation in response to LPS. Downregulation of Nox4 by transfection of siRNA specific to Nox4 in HAECs resulted in a failure to induce reactive oxygen species (ROS) generation and subsequent expression of intercellular adhesion molecule-1 (ICAM-1) and chemokines such as IL-8 and monocyte chemoattractant protein-1 (MCP-1) in response to LPS. Furthermore, transient transfection of endothelial cells with Nox4 siRNA led to a decrease in migration and adhesion of monocytes in response to LPS by 36% and 52%, respectively.
Nox4 plays a central role in LPS-induced proinflammatory responses by endothelial cells in an ROS-dependent manner.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>17064675</pmid><doi>10.1016/j.cardiores.2006.09.012</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Aorta Atherosclerosis (general aspects, experimental research) Bacterial Infections - enzymology Bacterial Infections - immunology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Adhesion - drug effects Cell Movement - drug effects Cell Nucleus - metabolism Cells, Cultured Chemokine CCL2 - analysis Endothelial Cells - enzymology Endothelial Cells - immunology Humans Hydrogen Peroxide - analysis Intercellular Adhesion Molecule-1 - analysis Interleukin-8 - analysis Lipopolysaccharides - pharmacology Medical sciences Monocytes - drug effects NADPH Oxidase 4 NADPH Oxidases - genetics NADPH Oxidases - physiology NF-kappa B - metabolism Protein Binding Reverse Transcriptase Polymerase Chain Reaction RNA Interference RNA, Small Interfering - pharmacology Transfection - methods Two-Hybrid System Techniques |
| title | Role of NADPH oxidase 4 in lipopolysaccharide-induced proinflammatory responses by human aortic endothelial cells |
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