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C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice
Plasma C-reactive protein (CRP) concentration is a strong predictor of atherosclerosis. However, to date, there is no in vivo evidence that CRP is proatherogenic. We studied the effect of human CRP transgene (tg) expression, under basal and turpentine-stimulated conditions, on atherosclerosis in apo...
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| Published in: | Circulation (New York, N.Y.) N.Y.), 2004-02, Vol.109 (5), p.647-655 |
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| cites | cdi_FETCH-LOGICAL-c531t-6dc3d2e397ba2a59dbc17425b86654bdc5c6dbe10680ddfc64ceb093e2a34b83 |
| container_end_page | 655 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | PAUL, Antoni KO, Kerry W. S LI, Lan YECHOOR, Vijay MCCRORY, Mark A SZALAI, Alexander J CHAN, Lawrence |
| description | Plasma C-reactive protein (CRP) concentration is a strong predictor of atherosclerosis. However, to date, there is no in vivo evidence that CRP is proatherogenic.
We studied the effect of human CRP transgene (tg) expression, under basal and turpentine-stimulated conditions, on atherosclerosis in apolipoprotein (apo) E-/- mice. Aortic atherosclerotic lesions in 29-week-old male mice were 48% larger (P |
| doi_str_mv | 10.1161/01.CIR.0000114526.50618.24 |
| format | article |
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We studied the effect of human CRP transgene (tg) expression, under basal and turpentine-stimulated conditions, on atherosclerosis in apolipoprotein (apo) E-/- mice. Aortic atherosclerotic lesions in 29-week-old male mice were 48% larger (P<0.02) in turpentine-treated mice and 34% larger (P<0.05) in untreated CRPtg+/0/apoE-/- mice. Turpentine treatment per se did not affect the extent of atherosclerosis in CRP transgenic or nontransgenic apoE-/- mice. Transgenic mice exhibited lower plasma complement C3 but increased deposition of CRP and C3 in the lesions, which suggests that CRP stimulated activation of complement within the lesion. There was more intense and widespread vascular cell adhesion molecule-1 and collagen staining in the lesions of CRPtg+/0/apoE-/- mice than in CRPtg0/0/apoE-/- littermates. Lesions of CRPtg+/0/apoE-/- mice contained increased angiotensin type 1 receptor (AT1-R) transcripts and displayed increased AT1-R immunostaining compared with those of CRPtg0/0/apoE-/- mice. There was no difference in blood pressure in the 2 types of mice, which indicates that the proatherogenic effect of CRP-associated AT1-R overexpression is local and not mediated by its hypertensive properties.
Human CRP transgene expression causes accelerated aortic atherosclerosis in apoE-/- mice. CRP was detected in the lesion, which was associated with increased C3 deposition and increased AT1-R, vascular cell adhesion molecule-1, and collagen expression. These data document a proatherogenic role for CRP in vivo.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000114526.50618.24</identifier><identifier>PMID: 14744975</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Aorta - chemistry ; Aorta - pathology ; Apolipoproteins E - genetics ; Arteriosclerosis - metabolism ; Arteriosclerosis - pathology ; Biological and medical sciences ; Blood and lymphatic vessels ; C-Reactive Protein - analysis ; C-Reactive Protein - genetics ; C-Reactive Protein - physiology ; Cardiology. Vascular system ; Complement C3 - analysis ; Disease Progression ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Humans ; Kinetics ; Male ; Medical sciences ; Mice ; Mice, Knockout ; Mice, Transgenic ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Phenotype ; Receptor, Angiotensin, Type 1 - metabolism ; Risk Factors</subject><ispartof>Circulation (New York, N.Y.), 2004-02, Vol.109 (5), p.647-655</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Feb 10 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c531t-6dc3d2e397ba2a59dbc17425b86654bdc5c6dbe10680ddfc64ceb093e2a34b83</citedby><cites>FETCH-LOGICAL-c531t-6dc3d2e397ba2a59dbc17425b86654bdc5c6dbe10680ddfc64ceb093e2a34b83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15461723$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14744975$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PAUL, Antoni</creatorcontrib><creatorcontrib>KO, Kerry W. S</creatorcontrib><creatorcontrib>LI, Lan</creatorcontrib><creatorcontrib>YECHOOR, Vijay</creatorcontrib><creatorcontrib>MCCRORY, Mark A</creatorcontrib><creatorcontrib>SZALAI, Alexander J</creatorcontrib><creatorcontrib>CHAN, Lawrence</creatorcontrib><title>C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Plasma C-reactive protein (CRP) concentration is a strong predictor of atherosclerosis. However, to date, there is no in vivo evidence that CRP is proatherogenic.
We studied the effect of human CRP transgene (tg) expression, under basal and turpentine-stimulated conditions, on atherosclerosis in apolipoprotein (apo) E-/- mice. Aortic atherosclerotic lesions in 29-week-old male mice were 48% larger (P<0.02) in turpentine-treated mice and 34% larger (P<0.05) in untreated CRPtg+/0/apoE-/- mice. Turpentine treatment per se did not affect the extent of atherosclerosis in CRP transgenic or nontransgenic apoE-/- mice. Transgenic mice exhibited lower plasma complement C3 but increased deposition of CRP and C3 in the lesions, which suggests that CRP stimulated activation of complement within the lesion. There was more intense and widespread vascular cell adhesion molecule-1 and collagen staining in the lesions of CRPtg+/0/apoE-/- mice than in CRPtg0/0/apoE-/- littermates. Lesions of CRPtg+/0/apoE-/- mice contained increased angiotensin type 1 receptor (AT1-R) transcripts and displayed increased AT1-R immunostaining compared with those of CRPtg0/0/apoE-/- mice. There was no difference in blood pressure in the 2 types of mice, which indicates that the proatherogenic effect of CRP-associated AT1-R overexpression is local and not mediated by its hypertensive properties.
Human CRP transgene expression causes accelerated aortic atherosclerosis in apoE-/- mice. CRP was detected in the lesion, which was associated with increased C3 deposition and increased AT1-R, vascular cell adhesion molecule-1, and collagen expression. These data document a proatherogenic role for CRP in vivo.</description><subject>Animals</subject><subject>Aorta - chemistry</subject><subject>Aorta - pathology</subject><subject>Apolipoproteins E - genetics</subject><subject>Arteriosclerosis - metabolism</subject><subject>Arteriosclerosis - pathology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>C-Reactive Protein - analysis</subject><subject>C-Reactive Protein - genetics</subject><subject>C-Reactive Protein - physiology</subject><subject>Cardiology. Vascular system</subject><subject>Complement C3 - analysis</subject><subject>Disease Progression</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Humans</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Phenotype</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Risk Factors</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNpdkdtKxDAQhoMouh5eQYqgd62ZHFvvZPEEgiDehzSZaqTbrklX8O3N6sqCuZiQ4fsnM_MTcga0AlBwSaGaPzxXNB8AIZmqJFVQV0zskBlIJkohebNLZhloSs0ZOyCHKb3np-Ja7pMDEFqIRssZ8fMyonVT-MRiGccJw1BY57DHaCdMxfT2k3-NmFIYh2LsCptzcUyuX8eQirViOfZhOf4VuCk9dsEFHKZiERwek73O9glPNvcRebm9eZnfl49Pdw_z68fSSQ5TqbzjniFvdGuZlY1vHWjBZFsrJUXrnXTKtwhU1dT7zinhsKUNR2a5aGt-RC5-y-Y-PlaYJrMIKY_S2wHHVTI1BaFYzTN49g98H1dxyK0ZBkxzraXI0NUv5PKYKWJnljEsbPwyQM3aB0PBZB_M1gfz44Nha_Hp5odVu0C_lW4Wn4HzDWCTs30X7eBC2nJSKNCM82-U0pKH</recordid><startdate>20040210</startdate><enddate>20040210</enddate><creator>PAUL, Antoni</creator><creator>KO, Kerry W. S</creator><creator>LI, Lan</creator><creator>YECHOOR, Vijay</creator><creator>MCCRORY, Mark A</creator><creator>SZALAI, Alexander J</creator><creator>CHAN, Lawrence</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>20040210</creationdate><title>C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice</title><author>PAUL, Antoni ; KO, Kerry W. S ; LI, Lan ; YECHOOR, Vijay ; MCCRORY, Mark A ; SZALAI, Alexander J ; CHAN, Lawrence</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c531t-6dc3d2e397ba2a59dbc17425b86654bdc5c6dbe10680ddfc64ceb093e2a34b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Aorta - chemistry</topic><topic>Aorta - pathology</topic><topic>Apolipoproteins E - genetics</topic><topic>Arteriosclerosis - metabolism</topic><topic>Arteriosclerosis - pathology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>C-Reactive Protein - analysis</topic><topic>C-Reactive Protein - genetics</topic><topic>C-Reactive Protein - physiology</topic><topic>Cardiology. Vascular system</topic><topic>Complement C3 - analysis</topic><topic>Disease Progression</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Humans</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Phenotype</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PAUL, Antoni</creatorcontrib><creatorcontrib>KO, Kerry W. S</creatorcontrib><creatorcontrib>LI, Lan</creatorcontrib><creatorcontrib>YECHOOR, Vijay</creatorcontrib><creatorcontrib>MCCRORY, Mark A</creatorcontrib><creatorcontrib>SZALAI, Alexander J</creatorcontrib><creatorcontrib>CHAN, Lawrence</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>PAUL, Antoni</au><au>KO, Kerry W. S</au><au>LI, Lan</au><au>YECHOOR, Vijay</au><au>MCCRORY, Mark A</au><au>SZALAI, Alexander J</au><au>CHAN, Lawrence</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2004-02-10</date><risdate>2004</risdate><volume>109</volume><issue>5</issue><spage>647</spage><epage>655</epage><pages>647-655</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Plasma C-reactive protein (CRP) concentration is a strong predictor of atherosclerosis. However, to date, there is no in vivo evidence that CRP is proatherogenic.
We studied the effect of human CRP transgene (tg) expression, under basal and turpentine-stimulated conditions, on atherosclerosis in apolipoprotein (apo) E-/- mice. Aortic atherosclerotic lesions in 29-week-old male mice were 48% larger (P<0.02) in turpentine-treated mice and 34% larger (P<0.05) in untreated CRPtg+/0/apoE-/- mice. Turpentine treatment per se did not affect the extent of atherosclerosis in CRP transgenic or nontransgenic apoE-/- mice. Transgenic mice exhibited lower plasma complement C3 but increased deposition of CRP and C3 in the lesions, which suggests that CRP stimulated activation of complement within the lesion. There was more intense and widespread vascular cell adhesion molecule-1 and collagen staining in the lesions of CRPtg+/0/apoE-/- mice than in CRPtg0/0/apoE-/- littermates. Lesions of CRPtg+/0/apoE-/- mice contained increased angiotensin type 1 receptor (AT1-R) transcripts and displayed increased AT1-R immunostaining compared with those of CRPtg0/0/apoE-/- mice. There was no difference in blood pressure in the 2 types of mice, which indicates that the proatherogenic effect of CRP-associated AT1-R overexpression is local and not mediated by its hypertensive properties.
Human CRP transgene expression causes accelerated aortic atherosclerosis in apoE-/- mice. CRP was detected in the lesion, which was associated with increased C3 deposition and increased AT1-R, vascular cell adhesion molecule-1, and collagen expression. These data document a proatherogenic role for CRP in vivo.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>14744975</pmid><doi>10.1161/01.CIR.0000114526.50618.24</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2004-02, Vol.109 (5), p.647-655 |
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| subjects | Animals Aorta - chemistry Aorta - pathology Apolipoproteins E - genetics Arteriosclerosis - metabolism Arteriosclerosis - pathology Biological and medical sciences Blood and lymphatic vessels C-Reactive Protein - analysis C-Reactive Protein - genetics C-Reactive Protein - physiology Cardiology. Vascular system Complement C3 - analysis Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Female Humans Kinetics Male Medical sciences Mice Mice, Knockout Mice, Transgenic Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Phenotype Receptor, Angiotensin, Type 1 - metabolism Risk Factors |
| title | C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice |
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