Influence of C3 deficiency on atherosclerosis
The influence of complement activation on atherosclerosis is not well understood. The purpose of this study was to examine the effects of C3 deficiency on the extent and phenotype of atherosclerosis. Aortic atherosclerosis was analyzed in low-density lipoprotein receptor (ldlr)/C3-deficient mice (ld...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-06, Vol.105 (25), p.3025-3031 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | BUONO, Chiara COME, Carolyn E WITZTUM, Joseph L MAGUIRE, Graham F CONNELLY, Philip W CARROLL, Michael LICHTMAN, Andrew H |
| description | The influence of complement activation on atherosclerosis is not well understood. The purpose of this study was to examine the effects of C3 deficiency on the extent and phenotype of atherosclerosis.
Aortic atherosclerosis was analyzed in low-density lipoprotein receptor (ldlr)/C3-deficient mice (ldlr(-/-)C3(-/-)) and ldlr(-/-)C3(+/-) littermate control mice after 15 weeks on a 1.25% (wt/wt) cholesterol diet. Serum lipoprotein profiles and immunoglobulin levels were not significantly different between the 2 experimental groups. The lipid-positive en face lesional area in thoracic and abdominal aorta was greater in C3-deficient mice than in control mice (3.9% versus 2.1%, median, P=0.0076). Similarly, the lipid-positive area in aortic arch sections was greater in C3-deficient mice than in controls (0.04 mm2 versus 0.02 mm2, median, P=0.0089). Analysis of aortic arch sections showed greater lesional macrophage content in C3-deficient versus control mice (8.24+/-1.36% versus 5.9+/-1.63% intimal area, mean+/-SEM, P=0.003), less smooth muscle cell content in C3-deficient versus control mice (0.06+/-0.05% versus 0.92+/-0.32% intimal area, mean+/-SEM, P |
| doi_str_mv | 10.1161/01.CIR.0000019584.04929.83 |
| format | Article |
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Aortic atherosclerosis was analyzed in low-density lipoprotein receptor (ldlr)/C3-deficient mice (ldlr(-/-)C3(-/-)) and ldlr(-/-)C3(+/-) littermate control mice after 15 weeks on a 1.25% (wt/wt) cholesterol diet. Serum lipoprotein profiles and immunoglobulin levels were not significantly different between the 2 experimental groups. The lipid-positive en face lesional area in thoracic and abdominal aorta was greater in C3-deficient mice than in control mice (3.9% versus 2.1%, median, P=0.0076). Similarly, the lipid-positive area in aortic arch sections was greater in C3-deficient mice than in controls (0.04 mm2 versus 0.02 mm2, median, P=0.0089). Analysis of aortic arch sections showed greater lesional macrophage content in C3-deficient versus control mice (8.24+/-1.36% versus 5.9+/-1.63% intimal area, mean+/-SEM, P=0.003), less smooth muscle cell content in C3-deficient versus control mice (0.06+/-0.05% versus 0.92+/-0.32% intimal area, mean+/-SEM, P<0.0001), and less collagen content in C3-deficient versus control mice (0.52+/-1.26% versus 11+/-10.43% intimal area, mean+/-SEM, P=0.008).
The maturation of atherosclerotic lesions beyond the foam cell stage is strongly dependent on an intact complement system.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000019584.04929.83</identifier><identifier>PMID: 12081998</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Aorta - pathology ; Arteriosclerosis - blood ; Arteriosclerosis - immunology ; Arteriosclerosis - pathology ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Complement C3 - genetics ; Complement C3 - physiology ; Immunoglobulins - blood ; Lipoproteins - blood ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phenotype ; Receptors, LDL - genetics</subject><ispartof>Circulation (New York, N.Y.), 2002-06, Vol.105 (25), p.3025-3031</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jun 25, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-3296106d80fe33b8858cf95236b092df59ceef6abd187512c795039260bbab7b3</citedby><cites>FETCH-LOGICAL-c590t-3296106d80fe33b8858cf95236b092df59ceef6abd187512c795039260bbab7b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,3674,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13764121$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12081998$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BUONO, Chiara</creatorcontrib><creatorcontrib>COME, Carolyn E</creatorcontrib><creatorcontrib>WITZTUM, Joseph L</creatorcontrib><creatorcontrib>MAGUIRE, Graham F</creatorcontrib><creatorcontrib>CONNELLY, Philip W</creatorcontrib><creatorcontrib>CARROLL, Michael</creatorcontrib><creatorcontrib>LICHTMAN, Andrew H</creatorcontrib><title>Influence of C3 deficiency on atherosclerosis</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The influence of complement activation on atherosclerosis is not well understood. The purpose of this study was to examine the effects of C3 deficiency on the extent and phenotype of atherosclerosis.
Aortic atherosclerosis was analyzed in low-density lipoprotein receptor (ldlr)/C3-deficient mice (ldlr(-/-)C3(-/-)) and ldlr(-/-)C3(+/-) littermate control mice after 15 weeks on a 1.25% (wt/wt) cholesterol diet. Serum lipoprotein profiles and immunoglobulin levels were not significantly different between the 2 experimental groups. The lipid-positive en face lesional area in thoracic and abdominal aorta was greater in C3-deficient mice than in control mice (3.9% versus 2.1%, median, P=0.0076). Similarly, the lipid-positive area in aortic arch sections was greater in C3-deficient mice than in controls (0.04 mm2 versus 0.02 mm2, median, P=0.0089). Analysis of aortic arch sections showed greater lesional macrophage content in C3-deficient versus control mice (8.24+/-1.36% versus 5.9+/-1.63% intimal area, mean+/-SEM, P=0.003), less smooth muscle cell content in C3-deficient versus control mice (0.06+/-0.05% versus 0.92+/-0.32% intimal area, mean+/-SEM, P<0.0001), and less collagen content in C3-deficient versus control mice (0.52+/-1.26% versus 11+/-10.43% intimal area, mean+/-SEM, P=0.008).
The maturation of atherosclerotic lesions beyond the foam cell stage is strongly dependent on an intact complement system.</description><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Arteriosclerosis - blood</subject><subject>Arteriosclerosis - immunology</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>Complement C3 - genetics</subject><subject>Complement C3 - physiology</subject><subject>Immunoglobulins - blood</subject><subject>Lipoproteins - blood</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Phenotype</subject><subject>Receptors, LDL - genetics</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkFtLwzAUgIMobk7_gpSBvrXmJM3NNyleBgNB9DkkaYIdXTub9WH_3swNBp6HHE7ynZPkQ2gOuADg8IChqBYfBd4HKCbLApeKqELSMzQFRsq8ZFSdo2k6V7mghEzQVYyrVHIq2CWaAMESlJJTlC-60I6-cz7rQ1bRrPahcU3a2GV9l5nttx_66Nr92sRrdBFMG_3NMc_Q18vzZ_WWL99fF9XTMndM4W1OieKAeS1x8JRaKZl0QTFCucWK1IEp533gxtYgBQPihGKYKsKxtcYKS2fo_jB3M_Q_o49bvW6i821rOt-PUQuQTCmMEzj_B676cejS2zQBwhMiIEGPB8ilT8TBB70ZmrUZdhqw3hvVGHQyqk9G9Z9RLWlqvj3eMNq1r0-tR4UJuDsCJjrThsF0roknjgpeAgH6CwIBfDE</recordid><startdate>20020625</startdate><enddate>20020625</enddate><creator>BUONO, Chiara</creator><creator>COME, Carolyn E</creator><creator>WITZTUM, Joseph L</creator><creator>MAGUIRE, Graham F</creator><creator>CONNELLY, Philip W</creator><creator>CARROLL, Michael</creator><creator>LICHTMAN, Andrew H</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>20020625</creationdate><title>Influence of C3 deficiency on atherosclerosis</title><author>BUONO, Chiara ; COME, Carolyn E ; WITZTUM, Joseph L ; MAGUIRE, Graham F ; CONNELLY, Philip W ; CARROLL, Michael ; LICHTMAN, Andrew H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-3296106d80fe33b8858cf95236b092df59ceef6abd187512c795039260bbab7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Arteriosclerosis - blood</topic><topic>Arteriosclerosis - immunology</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>Complement C3 - genetics</topic><topic>Complement C3 - physiology</topic><topic>Immunoglobulins - blood</topic><topic>Lipoproteins - blood</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Phenotype</topic><topic>Receptors, LDL - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BUONO, Chiara</creatorcontrib><creatorcontrib>COME, Carolyn E</creatorcontrib><creatorcontrib>WITZTUM, Joseph L</creatorcontrib><creatorcontrib>MAGUIRE, Graham F</creatorcontrib><creatorcontrib>CONNELLY, Philip W</creatorcontrib><creatorcontrib>CARROLL, Michael</creatorcontrib><creatorcontrib>LICHTMAN, Andrew H</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>BUONO, Chiara</au><au>COME, Carolyn E</au><au>WITZTUM, Joseph L</au><au>MAGUIRE, Graham F</au><au>CONNELLY, Philip W</au><au>CARROLL, Michael</au><au>LICHTMAN, Andrew H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of C3 deficiency on atherosclerosis</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-06-25</date><risdate>2002</risdate><volume>105</volume><issue>25</issue><spage>3025</spage><epage>3031</epage><pages>3025-3031</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>The influence of complement activation on atherosclerosis is not well understood. The purpose of this study was to examine the effects of C3 deficiency on the extent and phenotype of atherosclerosis.
Aortic atherosclerosis was analyzed in low-density lipoprotein receptor (ldlr)/C3-deficient mice (ldlr(-/-)C3(-/-)) and ldlr(-/-)C3(+/-) littermate control mice after 15 weeks on a 1.25% (wt/wt) cholesterol diet. Serum lipoprotein profiles and immunoglobulin levels were not significantly different between the 2 experimental groups. The lipid-positive en face lesional area in thoracic and abdominal aorta was greater in C3-deficient mice than in control mice (3.9% versus 2.1%, median, P=0.0076). Similarly, the lipid-positive area in aortic arch sections was greater in C3-deficient mice than in controls (0.04 mm2 versus 0.02 mm2, median, P=0.0089). Analysis of aortic arch sections showed greater lesional macrophage content in C3-deficient versus control mice (8.24+/-1.36% versus 5.9+/-1.63% intimal area, mean+/-SEM, P=0.003), less smooth muscle cell content in C3-deficient versus control mice (0.06+/-0.05% versus 0.92+/-0.32% intimal area, mean+/-SEM, P<0.0001), and less collagen content in C3-deficient versus control mice (0.52+/-1.26% versus 11+/-10.43% intimal area, mean+/-SEM, P=0.008).
The maturation of atherosclerotic lesions beyond the foam cell stage is strongly dependent on an intact complement system.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>12081998</pmid><doi>10.1161/01.CIR.0000019584.04929.83</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2002-06, Vol.105 (25), p.3025-3031 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Animals Aorta - pathology Arteriosclerosis - blood Arteriosclerosis - immunology Arteriosclerosis - pathology Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Complement C3 - genetics Complement C3 - physiology Immunoglobulins - blood Lipoproteins - blood Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Phenotype Receptors, LDL - genetics |
| title | Influence of C3 deficiency on atherosclerosis |
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