Statins Control Oxidized LDL-Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells
Activation of the endothelium by oxidized low-density lipoprotein (oxLDL) has been implicated in the development of atherosclerosis. Histone modifications impact on the transcriptional activity state of genes. We tested the hypothesis that oxLDL-induced inflammatory gene expression is regulated by h...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2009-03, Vol.29 (3), p.380-386 |
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| creator | N'GUESSAN, Philippe Dje RIEDIGER, Fabian SUTTORP, Norbert HIPPENSTIEL, Stefan VARDAROVA, Kremena SCHARF, Stefanie EITEL, Julia OPITZ, Bastian SLEVOGT, Hortense WEICHERT, Wilko HOCKE, Andreas C SCHMECK, Bernd |
| description | Activation of the endothelium by oxidized low-density lipoprotein (oxLDL) has been implicated in the development of atherosclerosis. Histone modifications impact on the transcriptional activity state of genes. We tested the hypothesis that oxLDL-induced inflammatory gene expression is regulated by histone modifications and experienced the effect of statins on these alterations.
OxLDL-related interleukin-8 (IL-8) and monocyte-chemoattractant protein-1 (MCP-1) secretion in endothelial cells was reduced by statins but enhanced by histone deacetylase inhibitors. OxLDL induced lectin-like oxidized LDL receptor-1 (LOX-1) and extracellular regulated kinases (ERK1/2)-dependent acetylation of histone H3 and H4 as well as phosphorylation of histone H3, both globally and on the promoters of il8 and mcp1. Pretreatment of oxLDL-exposed cells with statins reduced the above mentioned histone modification, as well as recruitment of CREB binding protein (CBP) 300, NF-kappaB, and of RNA polymerase II but prevented loss of binding of histone deacetylase (HDAC)-1 and -2 at the il8 and mcp1 gene promoters. OxLDL reduced HDAC1 and 2 expression, and statins partly restored global HDAC-activity. Statin-related effects were reverted with mevalonate. In situ experiments indicated decreased expression of HDAC2 in endothelial cells in atherosclerotic plaques of human coronary arteries.
Histone modifications seem to play an important role in atherosclerosis. |
| doi_str_mv | 10.1161/atvbaha.108.178319 |
| format | Article |
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OxLDL-related interleukin-8 (IL-8) and monocyte-chemoattractant protein-1 (MCP-1) secretion in endothelial cells was reduced by statins but enhanced by histone deacetylase inhibitors. OxLDL induced lectin-like oxidized LDL receptor-1 (LOX-1) and extracellular regulated kinases (ERK1/2)-dependent acetylation of histone H3 and H4 as well as phosphorylation of histone H3, both globally and on the promoters of il8 and mcp1. Pretreatment of oxLDL-exposed cells with statins reduced the above mentioned histone modification, as well as recruitment of CREB binding protein (CBP) 300, NF-kappaB, and of RNA polymerase II but prevented loss of binding of histone deacetylase (HDAC)-1 and -2 at the il8 and mcp1 gene promoters. OxLDL reduced HDAC1 and 2 expression, and statins partly restored global HDAC-activity. Statin-related effects were reverted with mevalonate. In situ experiments indicated decreased expression of HDAC2 in endothelial cells in atherosclerotic plaques of human coronary arteries.
Histone modifications seem to play an important role in atherosclerosis.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/atvbaha.108.178319</identifier><identifier>PMID: 19122173</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: Lippincott Williams & Wilkins</publisher><subject>Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Cardiology. Vascular system ; Cells, Cultured ; Chemokine CCL2 - metabolism ; Coronary Vessels - enzymology ; Cytokines - genetics ; Cytokines - metabolism ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Endothelial Cells - drug effects ; Endothelial Cells - enzymology ; Endothelial Cells - immunology ; Fatty Acids, Monounsaturated - pharmacology ; Fluvastatin ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Histone Deacetylase 1 ; Histone Deacetylase 2 ; Histone Deacetylase Inhibitors ; Histone Deacetylases - metabolism ; Histones - metabolism ; Humans ; Hydroxamic Acids - pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; Indoles - pharmacology ; Inflammation Mediators - metabolism ; Interleukin-8 - metabolism ; Lipoproteins, LDL - metabolism ; Medical sciences ; Mevalonic Acid - pharmacology ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Promoter Regions, Genetic - drug effects ; Repressor Proteins - antagonists & inhibitors ; Repressor Proteins - metabolism ; RNA Interference ; RNA, Small Interfering - metabolism ; Scavenger Receptors, Class E - metabolism ; Signal Transduction - drug effects ; Simvastatin - pharmacology ; Vertebrates: cardiovascular system ; Vorinostat</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2009-03, Vol.29 (3), p.380-386</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-17ee769478b8c78af7354fdd65c0156eb7de0e42147e8b8bfc92f3c71d92fff23</citedby><cites>FETCH-LOGICAL-c479t-17ee769478b8c78af7354fdd65c0156eb7de0e42147e8b8bfc92f3c71d92fff23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21172989$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19122173$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>N'GUESSAN, Philippe Dje</creatorcontrib><creatorcontrib>RIEDIGER, Fabian</creatorcontrib><creatorcontrib>SUTTORP, Norbert</creatorcontrib><creatorcontrib>HIPPENSTIEL, Stefan</creatorcontrib><creatorcontrib>VARDAROVA, Kremena</creatorcontrib><creatorcontrib>SCHARF, Stefanie</creatorcontrib><creatorcontrib>EITEL, Julia</creatorcontrib><creatorcontrib>OPITZ, Bastian</creatorcontrib><creatorcontrib>SLEVOGT, Hortense</creatorcontrib><creatorcontrib>WEICHERT, Wilko</creatorcontrib><creatorcontrib>HOCKE, Andreas C</creatorcontrib><creatorcontrib>SCHMECK, Bernd</creatorcontrib><title>Statins Control Oxidized LDL-Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>Activation of the endothelium by oxidized low-density lipoprotein (oxLDL) has been implicated in the development of atherosclerosis. Histone modifications impact on the transcriptional activity state of genes. We tested the hypothesis that oxLDL-induced inflammatory gene expression is regulated by histone modifications and experienced the effect of statins on these alterations.
OxLDL-related interleukin-8 (IL-8) and monocyte-chemoattractant protein-1 (MCP-1) secretion in endothelial cells was reduced by statins but enhanced by histone deacetylase inhibitors. OxLDL induced lectin-like oxidized LDL receptor-1 (LOX-1) and extracellular regulated kinases (ERK1/2)-dependent acetylation of histone H3 and H4 as well as phosphorylation of histone H3, both globally and on the promoters of il8 and mcp1. Pretreatment of oxLDL-exposed cells with statins reduced the above mentioned histone modification, as well as recruitment of CREB binding protein (CBP) 300, NF-kappaB, and of RNA polymerase II but prevented loss of binding of histone deacetylase (HDAC)-1 and -2 at the il8 and mcp1 gene promoters. OxLDL reduced HDAC1 and 2 expression, and statins partly restored global HDAC-activity. Statin-related effects were reverted with mevalonate. In situ experiments indicated decreased expression of HDAC2 in endothelial cells in atherosclerotic plaques of human coronary arteries.
Histone modifications seem to play an important role in atherosclerosis.</description><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>Cells, Cultured</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Coronary Vessels - enzymology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - enzymology</subject><subject>Endothelial Cells - immunology</subject><subject>Fatty Acids, Monounsaturated - pharmacology</subject><subject>Fluvastatin</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Histone Deacetylase 1</subject><subject>Histone Deacetylase 2</subject><subject>Histone Deacetylase Inhibitors</subject><subject>Histone Deacetylases - metabolism</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</subject><subject>Indoles - pharmacology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-8 - metabolism</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Medical sciences</subject><subject>Mevalonic Acid - pharmacology</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Promoter Regions, Genetic - drug effects</subject><subject>Repressor Proteins - antagonists & inhibitors</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Scavenger Receptors, Class E - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Simvastatin - pharmacology</subject><subject>Vertebrates: cardiovascular system</subject><subject>Vorinostat</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMFu1DAQhi1ERUvLC3BAvsAtW4_jxMlxSZcu0lY9tHCNHHusGmXtxXZQ4elxtSs4jWf0fb-sn5D3wFYALVyr_GtST2oFrFuB7GroX5ELaLioRFu3r8ubyb5qWsHPyduUfjDGBOfsDTmHHjgHWV-Q9JBVdj7RIfgcw0zvn51xf9DQ3c2uukPjVC7L1qUcPNK7YJx1uiihOMobeovlvHk-REypHKnzdFjmvMQXa9krTzfehPyEs1MzHXCe0xU5s2pO-O40L8m3L5vHYVvt7m-_DutdpYXscwUSUba9kN3UadkpK-tGWGPaRjNoWpykQYaCg5BYkMnqnttaSzBlWsvrS_LpmHuI4eeCKY97l3T5gfIYljS2JbyBjhWQH0EdQ0oR7XiIbq_i7xHY-FL1uH78_nm9XZe9G49VF-nDKX2Z9mj-K6duC_DxBKik1Wyj8tqlfxwHkLzv-vov3V-JRA</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>N'GUESSAN, Philippe Dje</creator><creator>RIEDIGER, Fabian</creator><creator>SUTTORP, Norbert</creator><creator>HIPPENSTIEL, Stefan</creator><creator>VARDAROVA, Kremena</creator><creator>SCHARF, Stefanie</creator><creator>EITEL, Julia</creator><creator>OPITZ, Bastian</creator><creator>SLEVOGT, Hortense</creator><creator>WEICHERT, Wilko</creator><creator>HOCKE, Andreas C</creator><creator>SCHMECK, Bernd</creator><general>Lippincott Williams & Wilkins</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>20090301</creationdate><title>Statins Control Oxidized LDL-Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells</title><author>N'GUESSAN, Philippe Dje ; RIEDIGER, Fabian ; SUTTORP, Norbert ; HIPPENSTIEL, Stefan ; VARDAROVA, Kremena ; SCHARF, Stefanie ; EITEL, Julia ; OPITZ, Bastian ; SLEVOGT, Hortense ; WEICHERT, Wilko ; HOCKE, Andreas C ; SCHMECK, Bernd</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-17ee769478b8c78af7354fdd65c0156eb7de0e42147e8b8bfc92f3c71d92fff23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><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>Cells, Cultured</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Coronary Vessels - enzymology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - enzymology</topic><topic>Endothelial Cells - immunology</topic><topic>Fatty Acids, Monounsaturated - pharmacology</topic><topic>Fluvastatin</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Histone Deacetylase 1</topic><topic>Histone Deacetylase 2</topic><topic>Histone Deacetylase Inhibitors</topic><topic>Histone Deacetylases - metabolism</topic><topic>Histones - metabolism</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</topic><topic>Indoles - pharmacology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-8 - metabolism</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Medical sciences</topic><topic>Mevalonic Acid - pharmacology</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Promoter Regions, Genetic - drug effects</topic><topic>Repressor Proteins - antagonists & inhibitors</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Scavenger Receptors, Class E - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Simvastatin - pharmacology</topic><topic>Vertebrates: cardiovascular system</topic><topic>Vorinostat</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>N'GUESSAN, Philippe Dje</creatorcontrib><creatorcontrib>RIEDIGER, Fabian</creatorcontrib><creatorcontrib>SUTTORP, Norbert</creatorcontrib><creatorcontrib>HIPPENSTIEL, Stefan</creatorcontrib><creatorcontrib>VARDAROVA, Kremena</creatorcontrib><creatorcontrib>SCHARF, Stefanie</creatorcontrib><creatorcontrib>EITEL, Julia</creatorcontrib><creatorcontrib>OPITZ, Bastian</creatorcontrib><creatorcontrib>SLEVOGT, Hortense</creatorcontrib><creatorcontrib>WEICHERT, Wilko</creatorcontrib><creatorcontrib>HOCKE, Andreas C</creatorcontrib><creatorcontrib>SCHMECK, Bernd</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>N'GUESSAN, Philippe Dje</au><au>RIEDIGER, Fabian</au><au>SUTTORP, Norbert</au><au>HIPPENSTIEL, Stefan</au><au>VARDAROVA, Kremena</au><au>SCHARF, Stefanie</au><au>EITEL, Julia</au><au>OPITZ, Bastian</au><au>SLEVOGT, Hortense</au><au>WEICHERT, Wilko</au><au>HOCKE, Andreas C</au><au>SCHMECK, Bernd</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Statins Control Oxidized LDL-Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>29</volume><issue>3</issue><spage>380</spage><epage>386</epage><pages>380-386</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>Activation of the endothelium by oxidized low-density lipoprotein (oxLDL) has been implicated in the development of atherosclerosis. Histone modifications impact on the transcriptional activity state of genes. We tested the hypothesis that oxLDL-induced inflammatory gene expression is regulated by histone modifications and experienced the effect of statins on these alterations.
OxLDL-related interleukin-8 (IL-8) and monocyte-chemoattractant protein-1 (MCP-1) secretion in endothelial cells was reduced by statins but enhanced by histone deacetylase inhibitors. OxLDL induced lectin-like oxidized LDL receptor-1 (LOX-1) and extracellular regulated kinases (ERK1/2)-dependent acetylation of histone H3 and H4 as well as phosphorylation of histone H3, both globally and on the promoters of il8 and mcp1. Pretreatment of oxLDL-exposed cells with statins reduced the above mentioned histone modification, as well as recruitment of CREB binding protein (CBP) 300, NF-kappaB, and of RNA polymerase II but prevented loss of binding of histone deacetylase (HDAC)-1 and -2 at the il8 and mcp1 gene promoters. OxLDL reduced HDAC1 and 2 expression, and statins partly restored global HDAC-activity. Statin-related effects were reverted with mevalonate. In situ experiments indicated decreased expression of HDAC2 in endothelial cells in atherosclerotic plaques of human coronary arteries.
Histone modifications seem to play an important role in atherosclerosis.</abstract><cop>Philadelphia, PA</cop><pub>Lippincott Williams & Wilkins</pub><pmid>19122173</pmid><doi>10.1161/atvbaha.108.178319</doi><tpages>7</tpages></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2009-03, Vol.29 (3), p.380-386 |
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| subjects | Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Cardiology. Vascular system Cells, Cultured Chemokine CCL2 - metabolism Coronary Vessels - enzymology Cytokines - genetics Cytokines - metabolism Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Endothelial Cells - drug effects Endothelial Cells - enzymology Endothelial Cells - immunology Fatty Acids, Monounsaturated - pharmacology Fluvastatin Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects Histone Deacetylase 1 Histone Deacetylase 2 Histone Deacetylase Inhibitors Histone Deacetylases - metabolism Histones - metabolism Humans Hydroxamic Acids - pharmacology Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Indoles - pharmacology Inflammation Mediators - metabolism Interleukin-8 - metabolism Lipoproteins, LDL - metabolism Medical sciences Mevalonic Acid - pharmacology Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Promoter Regions, Genetic - drug effects Repressor Proteins - antagonists & inhibitors Repressor Proteins - metabolism RNA Interference RNA, Small Interfering - metabolism Scavenger Receptors, Class E - metabolism Signal Transduction - drug effects Simvastatin - pharmacology Vertebrates: cardiovascular system Vorinostat |
| title | Statins Control Oxidized LDL-Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells |
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