A New Mechanism Involving ERK Contributes to Rosiglitazone Inhibition of Tumor Necrosis Factor-α and Interferon-γ Inflammatory Effects in Human Endothelial Cells
OBJECTIVE—Microvascular endothelium is one of the main targets of the inflammatory response. On specific activation, endothelial cells recruit Th1-lymphocytes at the inflammatory site. We investigated the intracellular signaling mediating tumor necrosis factor (TNF)-α and interferon (IFN)-γ inflamma...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2008-04, Vol.28 (4), p.718-724 |
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| creator | Lombardi, Adriana Cantini, Giulia Piscitelli, Elisabetta Gelmini, Stefania Francalanci, Michela Mello, Tommaso Ceni, Elisabetta Varano, Gabriele Forti, Gianni Rotondi, Mario Galli, Andrea Serio, Mario Luconi, Michaela |
| description | OBJECTIVE—Microvascular endothelium is one of the main targets of the inflammatory response. On specific activation, endothelial cells recruit Th1-lymphocytes at the inflammatory site. We investigated the intracellular signaling mediating tumor necrosis factor (TNF)-α and interferon (IFN)-γ inflammatory response in human microvascular endothelial cells (HMEC-1) and the interfering effects of the peroxisome-proliferator-activated-receptor (PPARγ) agonist, rosiglitazone (RGZ).
METHODS AND RESULTS—TNFα and IFNγ, mainly when combined, stimulate IFNγ-inducible protein of 10 kDa (IP10) and fractalkine production evaluated by ELISA and TaqMan analyses. This effect is not only mediated by activation of the NFkB and Stat1 classic pathways, but also involves a rapid increase in phosphorylation and activation of extracellular signal-regulated kinases (ERK1/2) as measured by Western blot. RGZ interferes with TNFα and IFNγ stimulation of IP10, fractalkine, and adhesion molecule through a novel rapid mechanism which involves the blocking of ERK activation.
CONCLUSIONS—Our findings shed new light on the mechanisms underlying the inflammatory response of microvascular endothelium and on the possible therapeutic use of RGZ in vasculopathies involving Th1-responses. |
| doi_str_mv | 10.1161/ATVBAHA.107.160713 |
| format | Article |
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METHODS AND RESULTS—TNFα and IFNγ, mainly when combined, stimulate IFNγ-inducible protein of 10 kDa (IP10) and fractalkine production evaluated by ELISA and TaqMan analyses. This effect is not only mediated by activation of the NFkB and Stat1 classic pathways, but also involves a rapid increase in phosphorylation and activation of extracellular signal-regulated kinases (ERK1/2) as measured by Western blot. RGZ interferes with TNFα and IFNγ stimulation of IP10, fractalkine, and adhesion molecule through a novel rapid mechanism which involves the blocking of ERK activation.
CONCLUSIONS—Our findings shed new light on the mechanisms underlying the inflammatory response of microvascular endothelium and on the possible therapeutic use of RGZ in vasculopathies involving Th1-responses.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/ATVBAHA.107.160713</identifier><identifier>PMID: 18239149</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Anti-Inflammatory Agents - metabolism ; Anti-Inflammatory Agents - pharmacology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Cardiology. Vascular system ; Cell Line ; Chemokine CXCL10 - metabolism ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Endothelial Cells - drug effects ; Endothelial Cells - immunology ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Fundamental and applied biological sciences. Psychology ; Humans ; Hypoglycemic Agents - metabolism ; Hypoglycemic Agents - pharmacology ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation - prevention & control ; Interferon-gamma - antagonists & inhibitors ; Interferon-gamma - biosynthesis ; MAP Kinase Signaling System - drug effects ; Medical sciences ; PPAR gamma - metabolism ; Signal Transduction - drug effects ; Th1 Cells - drug effects ; Th1 Cells - immunology ; Thiazolidinediones - metabolism ; Thiazolidinediones - pharmacology ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - biosynthesis ; Vertebrates: cardiovascular system</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2008-04, Vol.28 (4), p.718-724</ispartof><rights>2008 American Heart Association, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4201-ff43fb3fcdf825cb51d14660580c3988e9edcac227401585f02a41825b9a0ee93</citedby><cites>FETCH-LOGICAL-c4201-ff43fb3fcdf825cb51d14660580c3988e9edcac227401585f02a41825b9a0ee93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20217384$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18239149$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lombardi, Adriana</creatorcontrib><creatorcontrib>Cantini, Giulia</creatorcontrib><creatorcontrib>Piscitelli, Elisabetta</creatorcontrib><creatorcontrib>Gelmini, Stefania</creatorcontrib><creatorcontrib>Francalanci, Michela</creatorcontrib><creatorcontrib>Mello, Tommaso</creatorcontrib><creatorcontrib>Ceni, Elisabetta</creatorcontrib><creatorcontrib>Varano, Gabriele</creatorcontrib><creatorcontrib>Forti, Gianni</creatorcontrib><creatorcontrib>Rotondi, Mario</creatorcontrib><creatorcontrib>Galli, Andrea</creatorcontrib><creatorcontrib>Serio, Mario</creatorcontrib><creatorcontrib>Luconi, Michaela</creatorcontrib><title>A New Mechanism Involving ERK Contributes to Rosiglitazone Inhibition of Tumor Necrosis Factor-α and Interferon-γ Inflammatory Effects in Human Endothelial Cells</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Microvascular endothelium is one of the main targets of the inflammatory response. On specific activation, endothelial cells recruit Th1-lymphocytes at the inflammatory site. We investigated the intracellular signaling mediating tumor necrosis factor (TNF)-α and interferon (IFN)-γ inflammatory response in human microvascular endothelial cells (HMEC-1) and the interfering effects of the peroxisome-proliferator-activated-receptor (PPARγ) agonist, rosiglitazone (RGZ).
METHODS AND RESULTS—TNFα and IFNγ, mainly when combined, stimulate IFNγ-inducible protein of 10 kDa (IP10) and fractalkine production evaluated by ELISA and TaqMan analyses. This effect is not only mediated by activation of the NFkB and Stat1 classic pathways, but also involves a rapid increase in phosphorylation and activation of extracellular signal-regulated kinases (ERK1/2) as measured by Western blot. RGZ interferes with TNFα and IFNγ stimulation of IP10, fractalkine, and adhesion molecule through a novel rapid mechanism which involves the blocking of ERK activation.
CONCLUSIONS—Our findings shed new light on the mechanisms underlying the inflammatory response of microvascular endothelium and on the possible therapeutic use of RGZ in vasculopathies involving Th1-responses.</description><subject>Anti-Inflammatory Agents - metabolism</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Cardiology. Vascular system</subject><subject>Cell Line</subject><subject>Chemokine CXCL10 - metabolism</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - immunology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Hypoglycemic Agents - metabolism</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation - prevention & control</subject><subject>Interferon-gamma - antagonists & inhibitors</subject><subject>Interferon-gamma - biosynthesis</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Medical sciences</subject><subject>PPAR gamma - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Th1 Cells - drug effects</subject><subject>Th1 Cells - immunology</subject><subject>Thiazolidinediones - metabolism</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Vertebrates: cardiovascular system</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkU1uFDEQhVsIRELgAiyQN7DrofzTf8tmNGEiAkjRwLbldttpg9sOtjuj5Do5AeIeORMeTQsWJdeTvnpy1cuy1xhWGJf4fbv7_qHdtisM1QqXUGH6JDvFBWE5K2n5NPVQNXlRMnKSvQjhBwAwQuB5doJrQhvMmtPsoUVf5B59lmLkVocJXdhbZ261vUabq09o7Wz0up-jDCg6dOWCvjY68ntnZUJH3euonUVOod08OZ_MhE9QQOdcROfzx9-I2yGhUXolvbP545-klOHTxBNwhzZKSRED0hZt54lbtLGDi6M0mhu0lsaEl9kzxU2Qr5b3LPt2vtmtt_nl148X6_YyF4wAzpViVPVUiUHVpBB9gQfMyhKKGgRt6lo2chBcEFIxwEVdKCCcpUsUfcNByoaeZe-Ovjfe_ZpliN2kg0g_4Fa6OXRlDQ1u6iKB5Agedg1equ7G64n7uw5Dd4imW6JJuuqO0aShN4v73E9y-D-yZJGAtwvAg-BGeW6FDv84AgRXtGaJY0du70y6avhp5r303Si5iWN3CJmmpXMCUANLMk9FMP0LlnyqGg</recordid><startdate>200804</startdate><enddate>200804</enddate><creator>Lombardi, Adriana</creator><creator>Cantini, Giulia</creator><creator>Piscitelli, Elisabetta</creator><creator>Gelmini, Stefania</creator><creator>Francalanci, Michela</creator><creator>Mello, Tommaso</creator><creator>Ceni, Elisabetta</creator><creator>Varano, Gabriele</creator><creator>Forti, Gianni</creator><creator>Rotondi, Mario</creator><creator>Galli, Andrea</creator><creator>Serio, Mario</creator><creator>Luconi, Michaela</creator><general>American Heart Association, Inc</general><general>Lippincott</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>200804</creationdate><title>A New Mechanism Involving ERK Contributes to Rosiglitazone Inhibition of Tumor Necrosis Factor-α and Interferon-γ Inflammatory Effects in Human Endothelial Cells</title><author>Lombardi, Adriana ; Cantini, Giulia ; Piscitelli, Elisabetta ; Gelmini, Stefania ; Francalanci, Michela ; Mello, Tommaso ; Ceni, Elisabetta ; Varano, Gabriele ; Forti, Gianni ; Rotondi, Mario ; Galli, Andrea ; Serio, Mario ; Luconi, Michaela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4201-ff43fb3fcdf825cb51d14660580c3988e9edcac227401585f02a41825b9a0ee93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Anti-Inflammatory Agents - metabolism</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Cardiology. Vascular system</topic><topic>Cell Line</topic><topic>Chemokine CXCL10 - metabolism</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - immunology</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Hypoglycemic Agents - metabolism</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation - prevention & control</topic><topic>Interferon-gamma - antagonists & inhibitors</topic><topic>Interferon-gamma - biosynthesis</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Medical sciences</topic><topic>PPAR gamma - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Th1 Cells - drug effects</topic><topic>Th1 Cells - immunology</topic><topic>Thiazolidinediones - metabolism</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lombardi, Adriana</creatorcontrib><creatorcontrib>Cantini, Giulia</creatorcontrib><creatorcontrib>Piscitelli, Elisabetta</creatorcontrib><creatorcontrib>Gelmini, Stefania</creatorcontrib><creatorcontrib>Francalanci, Michela</creatorcontrib><creatorcontrib>Mello, Tommaso</creatorcontrib><creatorcontrib>Ceni, Elisabetta</creatorcontrib><creatorcontrib>Varano, Gabriele</creatorcontrib><creatorcontrib>Forti, Gianni</creatorcontrib><creatorcontrib>Rotondi, Mario</creatorcontrib><creatorcontrib>Galli, Andrea</creatorcontrib><creatorcontrib>Serio, Mario</creatorcontrib><creatorcontrib>Luconi, Michaela</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>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lombardi, Adriana</au><au>Cantini, Giulia</au><au>Piscitelli, Elisabetta</au><au>Gelmini, Stefania</au><au>Francalanci, Michela</au><au>Mello, Tommaso</au><au>Ceni, Elisabetta</au><au>Varano, Gabriele</au><au>Forti, Gianni</au><au>Rotondi, Mario</au><au>Galli, Andrea</au><au>Serio, Mario</au><au>Luconi, Michaela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A New Mechanism Involving ERK Contributes to Rosiglitazone Inhibition of Tumor Necrosis Factor-α and Interferon-γ Inflammatory Effects in Human Endothelial Cells</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2008-04</date><risdate>2008</risdate><volume>28</volume><issue>4</issue><spage>718</spage><epage>724</epage><pages>718-724</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—Microvascular endothelium is one of the main targets of the inflammatory response. On specific activation, endothelial cells recruit Th1-lymphocytes at the inflammatory site. We investigated the intracellular signaling mediating tumor necrosis factor (TNF)-α and interferon (IFN)-γ inflammatory response in human microvascular endothelial cells (HMEC-1) and the interfering effects of the peroxisome-proliferator-activated-receptor (PPARγ) agonist, rosiglitazone (RGZ).
METHODS AND RESULTS—TNFα and IFNγ, mainly when combined, stimulate IFNγ-inducible protein of 10 kDa (IP10) and fractalkine production evaluated by ELISA and TaqMan analyses. This effect is not only mediated by activation of the NFkB and Stat1 classic pathways, but also involves a rapid increase in phosphorylation and activation of extracellular signal-regulated kinases (ERK1/2) as measured by Western blot. RGZ interferes with TNFα and IFNγ stimulation of IP10, fractalkine, and adhesion molecule through a novel rapid mechanism which involves the blocking of ERK activation.
CONCLUSIONS—Our findings shed new light on the mechanisms underlying the inflammatory response of microvascular endothelium and on the possible therapeutic use of RGZ in vasculopathies involving Th1-responses.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>18239149</pmid><doi>10.1161/ATVBAHA.107.160713</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2008-04, Vol.28 (4), p.718-724 |
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| subjects | Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - pharmacology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Cardiology. Vascular system Cell Line Chemokine CXCL10 - metabolism Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Endothelial Cells - drug effects Endothelial Cells - immunology Endothelial Cells - metabolism Endothelial Cells - pathology Extracellular Signal-Regulated MAP Kinases - metabolism Fundamental and applied biological sciences. Psychology Humans Hypoglycemic Agents - metabolism Hypoglycemic Agents - pharmacology Inflammation - metabolism Inflammation - pathology Inflammation - prevention & control Interferon-gamma - antagonists & inhibitors Interferon-gamma - biosynthesis MAP Kinase Signaling System - drug effects Medical sciences PPAR gamma - metabolism Signal Transduction - drug effects Th1 Cells - drug effects Th1 Cells - immunology Thiazolidinediones - metabolism Thiazolidinediones - pharmacology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - biosynthesis Vertebrates: cardiovascular system |
| title | A New Mechanism Involving ERK Contributes to Rosiglitazone Inhibition of Tumor Necrosis Factor-α and Interferon-γ Inflammatory Effects in Human Endothelial Cells |
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