Direct anti-inflammatory mechanisms contribute to attenuation of experimental allograft arteriosclerosis by statins
Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. The interplay between host inflammatory cells and donor vascular wall cells results in an intimal hyperplastic lesion, which leads to isch...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2003-10, Vol.108 (17), p.2113-2120 |
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| creator | SHIMIZU, Koichi AIKAWA, Masanori TAKAYAMA, Kiyoshi LIBBY, Peter MITCHELL, Richard N |
| description | Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. The interplay between host inflammatory cells and donor vascular wall cells results in an intimal hyperplastic lesion, which leads to ischemia and graft failure. HMG-CoA reductase inhibitors (statins) reduce GAD in human cardiac allografts, although it is unclear whether this is secondary to cholesterol lowering or other mechanisms. This study tested the hypothesis that statins can suppress GAD by cholesterol-independent pathways.
We performed heterotopic murine cardiac transplants in total allogeneic or major histocompatibility complex class II-mismatched combinations. Transplanted animals received either control chow, chow containing 25 ppm cerivastatin (low dose), or chow containing 125 ppm cerivastatin (high dose). Mean plasma cerivastatin concentrations were 0.0 (control), 10.1 (low dose), and 21.9 (high dose) nmol/L, respectively. Plasma cholesterol levels were the same in all groups. GAD scores decreased in low-dose (P |
| doi_str_mv | 10.1161/01.CIR.0000092949.67153.74 |
| format | Article |
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We performed heterotopic murine cardiac transplants in total allogeneic or major histocompatibility complex class II-mismatched combinations. Transplanted animals received either control chow, chow containing 25 ppm cerivastatin (low dose), or chow containing 125 ppm cerivastatin (high dose). Mean plasma cerivastatin concentrations were 0.0 (control), 10.1 (low dose), and 21.9 (high dose) nmol/L, respectively. Plasma cholesterol levels were the same in all groups. GAD scores decreased in low-dose (P<0.05) and high-dose (P<0.0001) cerivastatin groups compared with controls, with concomitant reduction in graft-infiltrating cells and significantly decreased intragraft RANTES and monocyte chemotactic protein-1 mRNA expression. Cerivastatin, as well as other statins, also reduced RANTES and monocyte chemotactic protein-1 production in mouse endothelial cells stimulated with interferon-gamma and tumor necrosis factor-alpha in vitro.
Clinically achievable levels of an HMG-CoA reductase inhibitor attenuate GAD in murine heart transplants, diminish host inflammatory cell recruitment, and do not alter cholesterol levels. These results indicate that statins can affect arterial biology and inflammation independently of their effects on cholesterol metabolism.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000092949.67153.74</identifier><identifier>PMID: 14517172</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Arteriosclerosis - immunology ; Arteriosclerosis - pathology ; Arteriosclerosis - prevention & control ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Cells, Cultured ; Chemokine CCL2 - antagonists & inhibitors ; Chemokine CCL2 - biosynthesis ; Chemokine CCL5 - antagonists & inhibitors ; Chemokine CCL5 - biosynthesis ; Chemokines - genetics ; Cholesterol - blood ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Dose-Response Relationship, Drug ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Gene Expression - drug effects ; Graft Survival - drug effects ; Graft Survival - immunology ; Heart Transplantation - adverse effects ; Heart Transplantation - immunology ; Histocompatibility Antigens Class II - genetics ; Histocompatibility Antigens Class II - immunology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - blood ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Inflammation - immunology ; Inflammation - prevention & control ; Lymphocyte Culture Test, Mixed ; Macrophages - pathology ; Medical sciences ; Mice ; Mice, Inbred Strains ; Pyridines - blood ; Pyridines - therapeutic use ; RNA, Messenger - metabolism ; T-Lymphocytes - pathology ; Transplantation, Heterotopic ; Transplantation, Homologous - immunology ; Transplantation, Homologous - pathology</subject><ispartof>Circulation (New York, N.Y.), 2003-10, Vol.108 (17), p.2113-2120</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Oct 28 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c533t-2bed5c6dca38f8036b5727f5b11c15ac3a04b7d89c1589c92781ff06d6fa67c23</citedby><cites>FETCH-LOGICAL-c533t-2bed5c6dca38f8036b5727f5b11c15ac3a04b7d89c1589c92781ff06d6fa67c23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15231244$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14517172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHIMIZU, Koichi</creatorcontrib><creatorcontrib>AIKAWA, Masanori</creatorcontrib><creatorcontrib>TAKAYAMA, Kiyoshi</creatorcontrib><creatorcontrib>LIBBY, Peter</creatorcontrib><creatorcontrib>MITCHELL, Richard N</creatorcontrib><title>Direct anti-inflammatory mechanisms contribute to attenuation of experimental allograft arteriosclerosis by statins</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. The interplay between host inflammatory cells and donor vascular wall cells results in an intimal hyperplastic lesion, which leads to ischemia and graft failure. HMG-CoA reductase inhibitors (statins) reduce GAD in human cardiac allografts, although it is unclear whether this is secondary to cholesterol lowering or other mechanisms. This study tested the hypothesis that statins can suppress GAD by cholesterol-independent pathways.
We performed heterotopic murine cardiac transplants in total allogeneic or major histocompatibility complex class II-mismatched combinations. Transplanted animals received either control chow, chow containing 25 ppm cerivastatin (low dose), or chow containing 125 ppm cerivastatin (high dose). Mean plasma cerivastatin concentrations were 0.0 (control), 10.1 (low dose), and 21.9 (high dose) nmol/L, respectively. Plasma cholesterol levels were the same in all groups. GAD scores decreased in low-dose (P<0.05) and high-dose (P<0.0001) cerivastatin groups compared with controls, with concomitant reduction in graft-infiltrating cells and significantly decreased intragraft RANTES and monocyte chemotactic protein-1 mRNA expression. Cerivastatin, as well as other statins, also reduced RANTES and monocyte chemotactic protein-1 production in mouse endothelial cells stimulated with interferon-gamma and tumor necrosis factor-alpha in vitro.
Clinically achievable levels of an HMG-CoA reductase inhibitor attenuate GAD in murine heart transplants, diminish host inflammatory cell recruitment, and do not alter cholesterol levels. These results indicate that statins can affect arterial biology and inflammation independently of their effects on cholesterol metabolism.</description><subject>Animals</subject><subject>Arteriosclerosis - immunology</subject><subject>Arteriosclerosis - pathology</subject><subject>Arteriosclerosis - prevention & control</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - antagonists & inhibitors</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Chemokine CCL5 - antagonists & inhibitors</subject><subject>Chemokine CCL5 - biosynthesis</subject><subject>Chemokines - genetics</subject><subject>Cholesterol - blood</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Gene Expression - drug effects</subject><subject>Graft Survival - drug effects</subject><subject>Graft Survival - immunology</subject><subject>Heart Transplantation - adverse effects</subject><subject>Heart Transplantation - immunology</subject><subject>Histocompatibility Antigens Class II - genetics</subject><subject>Histocompatibility Antigens Class II - immunology</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - blood</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>Inflammation - immunology</subject><subject>Inflammation - prevention & control</subject><subject>Lymphocyte Culture Test, Mixed</subject><subject>Macrophages - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Pyridines - blood</subject><subject>Pyridines - therapeutic use</subject><subject>RNA, Messenger - metabolism</subject><subject>T-Lymphocytes - pathology</subject><subject>Transplantation, Heterotopic</subject><subject>Transplantation, Homologous - immunology</subject><subject>Transplantation, Homologous - pathology</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkduKFDEQhoMo7rj6ChIW9K7HVA6dae9kPC0sCKLXoTqdaJbuZEzSsPP2ZtyBAXORUJXvrwM_ITfAtgA9vGOw3d9-37LTGfggh22vQYmtlk_IBhSXnVRieEo2p_9OC86vyItS7lvYC62ekyuQCjRoviHlY8jOVoqxhi5EP-OyYE35SBdnf2MMZSnUplhzGNfqaE0Ua3VxxRpSpMlT93BwOSwuVpwpznP6ldG3grm2dCp2djmVUOh4pKU2VSwvyTOPc3Gvzu81-fn504_91-7u25fb_Ye7ziohasdHNynbTxbFzu-Y6EelufZqBLCg0ApkctTTbmhRuwaud-A966feY68tF9fk7WPdQ05_VleqWUKxbp4xurQWo0EAG4Rq4M1_4H1ac2yzGQ5cM8mGE_T-EbJtn5KdN4e2NuajAWZOvhgGpvliLr6Yf74YLZv49bnDOi5uukjPRjTgzRnAYnH2GaMN5cIpLoBLKf4CkzGZAg</recordid><startdate>20031028</startdate><enddate>20031028</enddate><creator>SHIMIZU, Koichi</creator><creator>AIKAWA, Masanori</creator><creator>TAKAYAMA, Kiyoshi</creator><creator>LIBBY, Peter</creator><creator>MITCHELL, Richard N</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20031028</creationdate><title>Direct anti-inflammatory mechanisms contribute to attenuation of experimental allograft arteriosclerosis by statins</title><author>SHIMIZU, Koichi ; AIKAWA, Masanori ; TAKAYAMA, Kiyoshi ; LIBBY, Peter ; MITCHELL, Richard N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c533t-2bed5c6dca38f8036b5727f5b11c15ac3a04b7d89c1589c92781ff06d6fa67c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Arteriosclerosis - immunology</topic><topic>Arteriosclerosis - pathology</topic><topic>Arteriosclerosis - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - antagonists & inhibitors</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Chemokine CCL5 - antagonists & inhibitors</topic><topic>Chemokine CCL5 - biosynthesis</topic><topic>Chemokines - genetics</topic><topic>Cholesterol - blood</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Gene Expression - drug effects</topic><topic>Graft Survival - drug effects</topic><topic>Graft Survival - immunology</topic><topic>Heart Transplantation - adverse effects</topic><topic>Heart Transplantation - immunology</topic><topic>Histocompatibility Antigens Class II - genetics</topic><topic>Histocompatibility Antigens Class II - immunology</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - blood</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>Inflammation - immunology</topic><topic>Inflammation - prevention & control</topic><topic>Lymphocyte Culture Test, Mixed</topic><topic>Macrophages - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Pyridines - blood</topic><topic>Pyridines - therapeutic use</topic><topic>RNA, Messenger - metabolism</topic><topic>T-Lymphocytes - pathology</topic><topic>Transplantation, Heterotopic</topic><topic>Transplantation, Homologous - immunology</topic><topic>Transplantation, Homologous - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHIMIZU, Koichi</creatorcontrib><creatorcontrib>AIKAWA, Masanori</creatorcontrib><creatorcontrib>TAKAYAMA, Kiyoshi</creatorcontrib><creatorcontrib>LIBBY, Peter</creatorcontrib><creatorcontrib>MITCHELL, Richard N</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><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHIMIZU, Koichi</au><au>AIKAWA, Masanori</au><au>TAKAYAMA, Kiyoshi</au><au>LIBBY, Peter</au><au>MITCHELL, Richard N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Direct anti-inflammatory mechanisms contribute to attenuation of experimental allograft arteriosclerosis by statins</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2003-10-28</date><risdate>2003</risdate><volume>108</volume><issue>17</issue><spage>2113</spage><epage>2120</epage><pages>2113-2120</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Despite the development of effective immunosuppressive therapy, transplant graft arterial disease (GAD) remains the major limitation to long-term graft survival. The interplay between host inflammatory cells and donor vascular wall cells results in an intimal hyperplastic lesion, which leads to ischemia and graft failure. HMG-CoA reductase inhibitors (statins) reduce GAD in human cardiac allografts, although it is unclear whether this is secondary to cholesterol lowering or other mechanisms. This study tested the hypothesis that statins can suppress GAD by cholesterol-independent pathways.
We performed heterotopic murine cardiac transplants in total allogeneic or major histocompatibility complex class II-mismatched combinations. Transplanted animals received either control chow, chow containing 25 ppm cerivastatin (low dose), or chow containing 125 ppm cerivastatin (high dose). Mean plasma cerivastatin concentrations were 0.0 (control), 10.1 (low dose), and 21.9 (high dose) nmol/L, respectively. Plasma cholesterol levels were the same in all groups. GAD scores decreased in low-dose (P<0.05) and high-dose (P<0.0001) cerivastatin groups compared with controls, with concomitant reduction in graft-infiltrating cells and significantly decreased intragraft RANTES and monocyte chemotactic protein-1 mRNA expression. Cerivastatin, as well as other statins, also reduced RANTES and monocyte chemotactic protein-1 production in mouse endothelial cells stimulated with interferon-gamma and tumor necrosis factor-alpha in vitro.
Clinically achievable levels of an HMG-CoA reductase inhibitor attenuate GAD in murine heart transplants, diminish host inflammatory cell recruitment, and do not alter cholesterol levels. These results indicate that statins can affect arterial biology and inflammation independently of their effects on cholesterol metabolism.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>14517172</pmid><doi>10.1161/01.CIR.0000092949.67153.74</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arteriosclerosis - immunology Arteriosclerosis - pathology Arteriosclerosis - prevention & control Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cells, Cultured Chemokine CCL2 - antagonists & inhibitors Chemokine CCL2 - biosynthesis Chemokine CCL5 - antagonists & inhibitors Chemokine CCL5 - biosynthesis Chemokines - genetics Cholesterol - blood Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Dose-Response Relationship, Drug Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Gene Expression - drug effects Graft Survival - drug effects Graft Survival - immunology Heart Transplantation - adverse effects Heart Transplantation - immunology Histocompatibility Antigens Class II - genetics Histocompatibility Antigens Class II - immunology Hydroxymethylglutaryl-CoA Reductase Inhibitors - blood Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Inflammation - immunology Inflammation - prevention & control Lymphocyte Culture Test, Mixed Macrophages - pathology Medical sciences Mice Mice, Inbred Strains Pyridines - blood Pyridines - therapeutic use RNA, Messenger - metabolism T-Lymphocytes - pathology Transplantation, Heterotopic Transplantation, Homologous - immunology Transplantation, Homologous - pathology |
| title | Direct anti-inflammatory mechanisms contribute to attenuation of experimental allograft arteriosclerosis by statins |
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