Monocyte Chemoattractant Protein-1 Is an Essential Inflammatory Mediator in Angiotensin II-Induced Progression of Established Atherosclerosis in Hypercholesterolemic Mice
OBJECTIVE—Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-03, Vol.24 (3), p.534-539 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Ni, Weihua Kitamoto, Shiro Ishibashi, Minako Usui, Makoto Inoue, Shujiro Hiasa, Ken-ichi Zhao, Qingwei Nishida, Ken-ichi Takeshita, Akira Egashira, Kensuke |
| description | OBJECTIVE—Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is implicated in atherogenesis by activating the vascular inflammation system, mainly through monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size and promotes destabilization of established atheromas by activating the monocyte chemoattractant protein-1 (MCP-1) pathway.
METHODS AND RESULTS—We report here that 4-week infusion of AngII not only increased plaque size but also induced a destabilization phenotype (ie, increased macrophages and lipids and decreased collagen and smooth muscle cells) of pre-existing atherosclerotic lesions of hypercholesterolemic mice. AngII also enhanced the gene expression of inflammatory cytokines (TNFα, IL-6, etc.) and chemokines (MCP-1, CCR2, etc). Blockade of MCP-1, by transfecting the deletion mutant of the human MCP-1 gene into the skeletal muscles, limited AngII-induced progression and destabilization of established atherosclerotic lesions and suppressed the induction of proinflammatory genes.
CONCLUSIONS—These data suggest that MCP-1 functions as a central inflammatory mediator in the AngII-induced progression and changes in plaque composition of established atheroma. |
| doi_str_mv | 10.1161/01.ATV.0000118275.60121.2b |
| format | Article |
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METHODS AND RESULTS—We report here that 4-week infusion of AngII not only increased plaque size but also induced a destabilization phenotype (ie, increased macrophages and lipids and decreased collagen and smooth muscle cells) of pre-existing atherosclerotic lesions of hypercholesterolemic mice. AngII also enhanced the gene expression of inflammatory cytokines (TNFα, IL-6, etc.) and chemokines (MCP-1, CCR2, etc). Blockade of MCP-1, by transfecting the deletion mutant of the human MCP-1 gene into the skeletal muscles, limited AngII-induced progression and destabilization of established atherosclerotic lesions and suppressed the induction of proinflammatory genes.
CONCLUSIONS—These data suggest that MCP-1 functions as a central inflammatory mediator in the AngII-induced progression and changes in plaque composition of established atheroma.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000118275.60121.2b</identifier><identifier>PMID: 14739122</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Angiotensin II - administration & dosage ; Angiotensin II - toxicity ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Animals ; Aortic Diseases - etiology ; Aortic Diseases - metabolism ; Aortic Diseases - pathology ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Arteriosclerosis - etiology ; Arteriosclerosis - metabolism ; Arteriosclerosis - pathology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Chemokine CCL2 - physiology ; Chemokines - biosynthesis ; Chemokines - genetics ; Cytokines - biosynthesis ; Cytokines - genetics ; Disease Progression ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Gene Expression Regulation - drug effects ; Gene Targeting ; Humans ; Hyperlipoproteinemia Type II - complications ; Imidazoles - pharmacology ; Inflammation ; Inflammation Mediators - physiology ; Injections, Intramuscular ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Olmesartan Medoxomil ; Random Allocation ; Recombinant Fusion Proteins - physiology ; Sequence Deletion ; Single-Blind Method ; Tetrazoles - pharmacology</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-03, Vol.24 (3), p.534-539</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Mar 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5706-a4c73bcad77ca17f3c693ba71b43b8473b00da919acc3f856c110788b74da1b03</citedby><cites>FETCH-LOGICAL-c5706-a4c73bcad77ca17f3c693ba71b43b8473b00da919acc3f856c110788b74da1b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27911,27912</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15590870$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14739122$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ni, Weihua</creatorcontrib><creatorcontrib>Kitamoto, Shiro</creatorcontrib><creatorcontrib>Ishibashi, Minako</creatorcontrib><creatorcontrib>Usui, Makoto</creatorcontrib><creatorcontrib>Inoue, Shujiro</creatorcontrib><creatorcontrib>Hiasa, Ken-ichi</creatorcontrib><creatorcontrib>Zhao, Qingwei</creatorcontrib><creatorcontrib>Nishida, Ken-ichi</creatorcontrib><creatorcontrib>Takeshita, Akira</creatorcontrib><creatorcontrib>Egashira, Kensuke</creatorcontrib><title>Monocyte Chemoattractant Protein-1 Is an Essential Inflammatory Mediator in Angiotensin II-Induced Progression of Established Atherosclerosis in Hypercholesterolemic Mice</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is implicated in atherogenesis by activating the vascular inflammation system, mainly through monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size and promotes destabilization of established atheromas by activating the monocyte chemoattractant protein-1 (MCP-1) pathway.
METHODS AND RESULTS—We report here that 4-week infusion of AngII not only increased plaque size but also induced a destabilization phenotype (ie, increased macrophages and lipids and decreased collagen and smooth muscle cells) of pre-existing atherosclerotic lesions of hypercholesterolemic mice. AngII also enhanced the gene expression of inflammatory cytokines (TNFα, IL-6, etc.) and chemokines (MCP-1, CCR2, etc). Blockade of MCP-1, by transfecting the deletion mutant of the human MCP-1 gene into the skeletal muscles, limited AngII-induced progression and destabilization of established atherosclerotic lesions and suppressed the induction of proinflammatory genes.
CONCLUSIONS—These data suggest that MCP-1 functions as a central inflammatory mediator in the AngII-induced progression and changes in plaque composition of established atheroma.</description><subject>Angiotensin II - administration & dosage</subject><subject>Angiotensin II - toxicity</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Animals</subject><subject>Aortic Diseases - etiology</subject><subject>Aortic Diseases - metabolism</subject><subject>Aortic Diseases - pathology</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</subject><subject>Arteriosclerosis - etiology</subject><subject>Arteriosclerosis - metabolism</subject><subject>Arteriosclerosis - pathology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Chemokine CCL2 - physiology</subject><subject>Chemokines - biosynthesis</subject><subject>Chemokines - genetics</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - genetics</subject><subject>Disease Progression</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Targeting</subject><subject>Humans</subject><subject>Hyperlipoproteinemia Type II - complications</subject><subject>Imidazoles - pharmacology</subject><subject>Inflammation</subject><subject>Inflammation Mediators - physiology</subject><subject>Injections, Intramuscular</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Olmesartan Medoxomil</subject><subject>Random Allocation</subject><subject>Recombinant Fusion Proteins - physiology</subject><subject>Sequence Deletion</subject><subject>Single-Blind Method</subject><subject>Tetrazoles - pharmacology</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUV2P1CAUbYzGXVf_giGb-NjKR0tb3yaT1W2yE31YfSVA6ZaVwghMNvOX_JXeOpMMCXCAc8-93FMUtwRXhHDyGZNq8_irwjAI6WjbVBwTSiqqXhXXpKF1WXPGXwPGbV82vKZXxbuUnoFfU4rfFlekbllPKL0u_u6CD_qYDdrOZgky5yh1lj6jHzFkY31J0JCQ9OguJeOzlQ4NfnJyWWQO8Yh2ZrQrQtajjX-yEOQT4GEoBz8etBlXpadoUrLBozCBUJbK2TTD0ybPJoak3bratIrcH_cm6jk4kzLcOrNYjXZWm_fFm0m6ZD6c95vi59e7x-19-fD927DdPJS6aTEvZa1bprQc21ZL0k5M854p2RJVM9XBxxXGo-xJL7VmU9dwTaBPXafaepREYXZT3J509zH8OUAV4jkcooeUgkIDO8Y5A9KXE0lD4SmaSeyjXWQ8CoLF6pLARIBL4uKS-O-SoAqCP54zHNRixkvo2RYgfDoTZNLSTVF6bdOF1zQ97tq11PrEewkOmpV-u8OLiWI20uV5TV0zjpuSAsAMjiVMytk_cgeuWQ</recordid><startdate>200403</startdate><enddate>200403</enddate><creator>Ni, Weihua</creator><creator>Kitamoto, Shiro</creator><creator>Ishibashi, Minako</creator><creator>Usui, Makoto</creator><creator>Inoue, Shujiro</creator><creator>Hiasa, Ken-ichi</creator><creator>Zhao, Qingwei</creator><creator>Nishida, Ken-ichi</creator><creator>Takeshita, Akira</creator><creator>Egashira, Kensuke</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>K9.</scope></search><sort><creationdate>200403</creationdate><title>Monocyte Chemoattractant Protein-1 Is an Essential Inflammatory Mediator in Angiotensin II-Induced Progression of Established Atherosclerosis in Hypercholesterolemic Mice</title><author>Ni, Weihua ; Kitamoto, Shiro ; Ishibashi, Minako ; Usui, Makoto ; Inoue, Shujiro ; Hiasa, Ken-ichi ; Zhao, Qingwei ; Nishida, Ken-ichi ; Takeshita, Akira ; Egashira, Kensuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5706-a4c73bcad77ca17f3c693ba71b43b8473b00da919acc3f856c110788b74da1b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Angiotensin II - administration & dosage</topic><topic>Angiotensin II - toxicity</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Animals</topic><topic>Aortic Diseases - etiology</topic><topic>Aortic Diseases - metabolism</topic><topic>Aortic Diseases - pathology</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - genetics</topic><topic>Arteriosclerosis - etiology</topic><topic>Arteriosclerosis - metabolism</topic><topic>Arteriosclerosis - pathology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Chemokine CCL2 - physiology</topic><topic>Chemokines - biosynthesis</topic><topic>Chemokines - genetics</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - genetics</topic><topic>Disease Progression</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Targeting</topic><topic>Humans</topic><topic>Hyperlipoproteinemia Type II - complications</topic><topic>Imidazoles - pharmacology</topic><topic>Inflammation</topic><topic>Inflammation Mediators - physiology</topic><topic>Injections, Intramuscular</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Olmesartan Medoxomil</topic><topic>Random Allocation</topic><topic>Recombinant Fusion Proteins - physiology</topic><topic>Sequence Deletion</topic><topic>Single-Blind Method</topic><topic>Tetrazoles - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ni, Weihua</creatorcontrib><creatorcontrib>Kitamoto, Shiro</creatorcontrib><creatorcontrib>Ishibashi, Minako</creatorcontrib><creatorcontrib>Usui, Makoto</creatorcontrib><creatorcontrib>Inoue, Shujiro</creatorcontrib><creatorcontrib>Hiasa, Ken-ichi</creatorcontrib><creatorcontrib>Zhao, Qingwei</creatorcontrib><creatorcontrib>Nishida, Ken-ichi</creatorcontrib><creatorcontrib>Takeshita, Akira</creatorcontrib><creatorcontrib>Egashira, Kensuke</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>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ni, Weihua</au><au>Kitamoto, Shiro</au><au>Ishibashi, Minako</au><au>Usui, Makoto</au><au>Inoue, Shujiro</au><au>Hiasa, Ken-ichi</au><au>Zhao, Qingwei</au><au>Nishida, Ken-ichi</au><au>Takeshita, Akira</au><au>Egashira, Kensuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monocyte Chemoattractant Protein-1 Is an Essential Inflammatory Mediator in Angiotensin II-Induced Progression of Established Atherosclerosis in Hypercholesterolemic Mice</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-03</date><risdate>2004</risdate><volume>24</volume><issue>3</issue><spage>534</spage><epage>539</epage><pages>534-539</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is implicated in atherogenesis by activating the vascular inflammation system, mainly through monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size and promotes destabilization of established atheromas by activating the monocyte chemoattractant protein-1 (MCP-1) pathway.
METHODS AND RESULTS—We report here that 4-week infusion of AngII not only increased plaque size but also induced a destabilization phenotype (ie, increased macrophages and lipids and decreased collagen and smooth muscle cells) of pre-existing atherosclerotic lesions of hypercholesterolemic mice. AngII also enhanced the gene expression of inflammatory cytokines (TNFα, IL-6, etc.) and chemokines (MCP-1, CCR2, etc). Blockade of MCP-1, by transfecting the deletion mutant of the human MCP-1 gene into the skeletal muscles, limited AngII-induced progression and destabilization of established atherosclerotic lesions and suppressed the induction of proinflammatory genes.
CONCLUSIONS—These data suggest that MCP-1 functions as a central inflammatory mediator in the AngII-induced progression and changes in plaque composition of established atheroma.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>14739122</pmid><doi>10.1161/01.ATV.0000118275.60121.2b</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2004-03, Vol.24 (3), p.534-539 |
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| subjects | Angiotensin II - administration & dosage Angiotensin II - toxicity Angiotensin II Type 1 Receptor Blockers - pharmacology Animals Aortic Diseases - etiology Aortic Diseases - metabolism Aortic Diseases - pathology Apolipoproteins E - deficiency Apolipoproteins E - genetics Arteriosclerosis - etiology Arteriosclerosis - metabolism Arteriosclerosis - pathology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Chemokine CCL2 - physiology Chemokines - biosynthesis Chemokines - genetics Cytokines - biosynthesis Cytokines - genetics Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Gene Expression Regulation - drug effects Gene Targeting Humans Hyperlipoproteinemia Type II - complications Imidazoles - pharmacology Inflammation Inflammation Mediators - physiology Injections, Intramuscular Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Olmesartan Medoxomil Random Allocation Recombinant Fusion Proteins - physiology Sequence Deletion Single-Blind Method Tetrazoles - pharmacology |
| title | Monocyte Chemoattractant Protein-1 Is an Essential Inflammatory Mediator in Angiotensin II-Induced Progression of Established Atherosclerosis in Hypercholesterolemic Mice |
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