Anti-atherosclerotic effect of simvastatin depends on the presence of apolipoprotein E
Low density lipoprotein receptor deficient (LDLR-KO) and apolipoprotein E deficient (apo E-KO) mice both develop hyperlipidemia and atherosclerosis by different mechanisms. The aim of the present study was to compare the effects of simvastatin on cholesterol levels, endothelial dysfunction, and aort...
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| Veröffentlicht in: | Atherosclerosis 2002-05, Vol.162 (1), p.23-31 |
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| creator | Wang, Yi-Xin (Jim) Martin-McNulty, Baby Huw, Ling-Yuh da Cunha, Valdeci Post, Joe Hinchman, Josephine Vergona, Ronald Sullivan, Mark E. Dole, William Kauser, Katalin |
| description | Low density lipoprotein receptor deficient (LDLR-KO) and apolipoprotein E deficient (apo E-KO) mice both develop hyperlipidemia and atherosclerosis by different mechanisms. The aim of the present study was to compare the effects of simvastatin on cholesterol levels, endothelial dysfunction, and aortic lesions in these two models of experimental atherosclerosis. Male LDLR-KO mice fed a high cholesterol (HC; 1%) diet developed atherosclerosis at 8 months of age with hypercholesterolemia. The addition of simvastatin (300 mg/kg daily) to the HC diet for 2 more months lowered total cholesterol levels by ∼57% and reduced aortic plaque area by ∼15% compared with the LDLR-KO mice continued on HC diet alone,
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| doi_str_mv | 10.1016/S0021-9150(01)00678-5 |
| format | Article |
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P<0.05. Simvastatin treatment also improved acetylcholine (ACh)-induced endothelium-dependent vasorelaxation in isolated aortic rings, which was associated with an increase in NOS-3 expression by ∼88% in the aorta measured by real time polymerase chain reaction (PCR),
P<0.05. In contrast, in age-matched male apo E-KO mice fed a normal diet, the same treatment of simvastatin elevated serum total cholesterol by ∼35%, increased aortic plaque area by ∼15%, and had no effect on endothelial function. These results suggest that the therapeutic effects of simvastatin may depend on the presence of a functional apolipoprotein E.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/S0021-9150(01)00678-5</identifier><identifier>PMID: 11947894</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Acetylcholine - pharmacology ; Animals ; Aorta - pathology ; Apo E-knockout ; Apolipoproteins E - deficiency ; Apolipoproteins E - drug effects ; Arteriosclerosis - blood ; Arteriosclerosis - drug therapy ; Arteriosclerosis - etiology ; Atherosclerotic plaque ; Biological and medical sciences ; Cholesterol ; Cholesterol, HDL - blood ; Cholesterol, HDL - drug effects ; Cholesterol, LDL - blood ; Cholesterol, LDL - drug effects ; Disease Models, Animal ; Endothelial dysfunction ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; General and cellular metabolism. Vitamins ; HMG-CoA reductase inhibitor ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Hypercholesterolemia - blood ; Hypercholesterolemia - drug therapy ; Hypercholesterolemia - etiology ; LDLR-knockout ; Male ; Medical sciences ; Mice ; Mice, Knockout ; Models, Cardiovascular ; Mouse ; Muscle Relaxation - drug effects ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - biosynthesis ; Nitric Oxide Synthase - drug effects ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; NOS-3 ; Pharmacology. Drug treatments ; Receptors, LDL - deficiency ; Receptors, LDL - drug effects ; RNA, Messenger - biosynthesis ; RNA, Messenger - drug effects ; Simvastatin - therapeutic use ; Treatment Outcome ; Triglycerides - blood ; Vasodilator Agents - pharmacology</subject><ispartof>Atherosclerosis, 2002-05, Vol.162 (1), p.23-31</ispartof><rights>2002 Elsevier Science Ireland Ltd</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-2da1de80168bb40859bd25c3a7cfe83d9721016e12ca98f556245922b69132d93</citedby><cites>FETCH-LOGICAL-c509t-2da1de80168bb40859bd25c3a7cfe83d9721016e12ca98f556245922b69132d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021915001006785$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13603047$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11947894$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yi-Xin (Jim)</creatorcontrib><creatorcontrib>Martin-McNulty, Baby</creatorcontrib><creatorcontrib>Huw, Ling-Yuh</creatorcontrib><creatorcontrib>da Cunha, Valdeci</creatorcontrib><creatorcontrib>Post, Joe</creatorcontrib><creatorcontrib>Hinchman, Josephine</creatorcontrib><creatorcontrib>Vergona, Ronald</creatorcontrib><creatorcontrib>Sullivan, Mark E.</creatorcontrib><creatorcontrib>Dole, William</creatorcontrib><creatorcontrib>Kauser, Katalin</creatorcontrib><title>Anti-atherosclerotic effect of simvastatin depends on the presence of apolipoprotein E</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Low density lipoprotein receptor deficient (LDLR-KO) and apolipoprotein E deficient (apo E-KO) mice both develop hyperlipidemia and atherosclerosis by different mechanisms. The aim of the present study was to compare the effects of simvastatin on cholesterol levels, endothelial dysfunction, and aortic lesions in these two models of experimental atherosclerosis. Male LDLR-KO mice fed a high cholesterol (HC; 1%) diet developed atherosclerosis at 8 months of age with hypercholesterolemia. The addition of simvastatin (300 mg/kg daily) to the HC diet for 2 more months lowered total cholesterol levels by ∼57% and reduced aortic plaque area by ∼15% compared with the LDLR-KO mice continued on HC diet alone,
P<0.05. Simvastatin treatment also improved acetylcholine (ACh)-induced endothelium-dependent vasorelaxation in isolated aortic rings, which was associated with an increase in NOS-3 expression by ∼88% in the aorta measured by real time polymerase chain reaction (PCR),
P<0.05. In contrast, in age-matched male apo E-KO mice fed a normal diet, the same treatment of simvastatin elevated serum total cholesterol by ∼35%, increased aortic plaque area by ∼15%, and had no effect on endothelial function. These results suggest that the therapeutic effects of simvastatin may depend on the presence of a functional apolipoprotein E.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Apo E-knockout</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - drug effects</subject><subject>Arteriosclerosis - blood</subject><subject>Arteriosclerosis - drug therapy</subject><subject>Arteriosclerosis - etiology</subject><subject>Atherosclerotic plaque</subject><subject>Biological and medical sciences</subject><subject>Cholesterol</subject><subject>Cholesterol, HDL - blood</subject><subject>Cholesterol, HDL - drug effects</subject><subject>Cholesterol, LDL - blood</subject><subject>Cholesterol, LDL - drug effects</subject><subject>Disease Models, Animal</subject><subject>Endothelial dysfunction</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>General and cellular metabolism. Vitamins</subject><subject>HMG-CoA reductase inhibitor</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>Hypercholesterolemia - blood</subject><subject>Hypercholesterolemia - drug therapy</subject><subject>Hypercholesterolemia - etiology</subject><subject>LDLR-knockout</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Models, Cardiovascular</subject><subject>Mouse</subject><subject>Muscle Relaxation - drug effects</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - biosynthesis</subject><subject>Nitric Oxide Synthase - drug effects</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitric Oxide Synthase Type III</subject><subject>NOS-3</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptors, LDL - deficiency</subject><subject>Receptors, LDL - drug effects</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - drug effects</subject><subject>Simvastatin - therapeutic use</subject><subject>Treatment Outcome</subject><subject>Triglycerides - blood</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkL1OwzAYRS0EoqXwCKAsIBgC_pw4sSdUVeVHqsTAz2o59hdhlCYhTivx9jhtRUcWeznX1_cQcg70Fihkd6-UMoglcHpN4YbSLBcxPyBjELmMIRXpIRn_ISNy4v0XpTTNQRyTEYBMcyHTMfmY1r2Ldf-JXeNNFc7emQjLEk0fNWXk3XKtfa97V0cWW6ytj5o6CnzUduixNjhgum0q1zZtiGMg56fkqNSVx7PdPSHvD_O32VO8eHl8nk0XseFU9jGzGiyKsEcURUoFl4Vl3CQ6NyWKxMqcDWMRmNFSlJxnLOWSsSKTkDArkwm52r4bmr9X6Hu1dN5gVekam5VXOXDBBSQB5FvQhJ2-w1K1nVvq7kcBVUOH2ghVgy1FQW2EKh5yF7uCVbFEu0_tDAbgcgdob3RVdro2zu-5JKNJ0B64-y2HQcfaYae8cYM-67rgWtnG_fOVXzXhkek</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Wang, Yi-Xin (Jim)</creator><creator>Martin-McNulty, Baby</creator><creator>Huw, Ling-Yuh</creator><creator>da Cunha, Valdeci</creator><creator>Post, Joe</creator><creator>Hinchman, Josephine</creator><creator>Vergona, Ronald</creator><creator>Sullivan, Mark E.</creator><creator>Dole, William</creator><creator>Kauser, Katalin</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</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>20020501</creationdate><title>Anti-atherosclerotic effect of simvastatin depends on the presence of apolipoprotein E</title><author>Wang, Yi-Xin (Jim) ; Martin-McNulty, Baby ; Huw, Ling-Yuh ; da Cunha, Valdeci ; Post, Joe ; Hinchman, Josephine ; Vergona, Ronald ; Sullivan, Mark E. ; Dole, William ; Kauser, Katalin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-2da1de80168bb40859bd25c3a7cfe83d9721016e12ca98f556245922b69132d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Apo E-knockout</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - drug effects</topic><topic>Arteriosclerosis - blood</topic><topic>Arteriosclerosis - drug therapy</topic><topic>Arteriosclerosis - etiology</topic><topic>Atherosclerotic plaque</topic><topic>Biological and medical sciences</topic><topic>Cholesterol</topic><topic>Cholesterol, HDL - blood</topic><topic>Cholesterol, HDL - drug effects</topic><topic>Cholesterol, LDL - blood</topic><topic>Cholesterol, LDL - drug effects</topic><topic>Disease Models, Animal</topic><topic>Endothelial dysfunction</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>General and cellular metabolism. Vitamins</topic><topic>HMG-CoA reductase inhibitor</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>Hypercholesterolemia - blood</topic><topic>Hypercholesterolemia - drug therapy</topic><topic>Hypercholesterolemia - etiology</topic><topic>LDLR-knockout</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Models, Cardiovascular</topic><topic>Mouse</topic><topic>Muscle Relaxation - drug effects</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - biosynthesis</topic><topic>Nitric Oxide Synthase - drug effects</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nitric Oxide Synthase Type III</topic><topic>NOS-3</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptors, LDL - deficiency</topic><topic>Receptors, LDL - drug effects</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - drug effects</topic><topic>Simvastatin - therapeutic use</topic><topic>Treatment Outcome</topic><topic>Triglycerides - blood</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yi-Xin (Jim)</creatorcontrib><creatorcontrib>Martin-McNulty, Baby</creatorcontrib><creatorcontrib>Huw, Ling-Yuh</creatorcontrib><creatorcontrib>da Cunha, Valdeci</creatorcontrib><creatorcontrib>Post, Joe</creatorcontrib><creatorcontrib>Hinchman, Josephine</creatorcontrib><creatorcontrib>Vergona, Ronald</creatorcontrib><creatorcontrib>Sullivan, Mark E.</creatorcontrib><creatorcontrib>Dole, William</creatorcontrib><creatorcontrib>Kauser, Katalin</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>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yi-Xin (Jim)</au><au>Martin-McNulty, Baby</au><au>Huw, Ling-Yuh</au><au>da Cunha, Valdeci</au><au>Post, Joe</au><au>Hinchman, Josephine</au><au>Vergona, Ronald</au><au>Sullivan, Mark E.</au><au>Dole, William</au><au>Kauser, Katalin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-atherosclerotic effect of simvastatin depends on the presence of apolipoprotein E</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2002-05-01</date><risdate>2002</risdate><volume>162</volume><issue>1</issue><spage>23</spage><epage>31</epage><pages>23-31</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Low density lipoprotein receptor deficient (LDLR-KO) and apolipoprotein E deficient (apo E-KO) mice both develop hyperlipidemia and atherosclerosis by different mechanisms. The aim of the present study was to compare the effects of simvastatin on cholesterol levels, endothelial dysfunction, and aortic lesions in these two models of experimental atherosclerosis. Male LDLR-KO mice fed a high cholesterol (HC; 1%) diet developed atherosclerosis at 8 months of age with hypercholesterolemia. The addition of simvastatin (300 mg/kg daily) to the HC diet for 2 more months lowered total cholesterol levels by ∼57% and reduced aortic plaque area by ∼15% compared with the LDLR-KO mice continued on HC diet alone,
P<0.05. Simvastatin treatment also improved acetylcholine (ACh)-induced endothelium-dependent vasorelaxation in isolated aortic rings, which was associated with an increase in NOS-3 expression by ∼88% in the aorta measured by real time polymerase chain reaction (PCR),
P<0.05. In contrast, in age-matched male apo E-KO mice fed a normal diet, the same treatment of simvastatin elevated serum total cholesterol by ∼35%, increased aortic plaque area by ∼15%, and had no effect on endothelial function. These results suggest that the therapeutic effects of simvastatin may depend on the presence of a functional apolipoprotein E.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>11947894</pmid><doi>10.1016/S0021-9150(01)00678-5</doi><tpages>9</tpages></addata></record> |
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| ispartof | Atherosclerosis, 2002-05, Vol.162 (1), p.23-31 |
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| subjects | Acetylcholine - pharmacology Animals Aorta - pathology Apo E-knockout Apolipoproteins E - deficiency Apolipoproteins E - drug effects Arteriosclerosis - blood Arteriosclerosis - drug therapy Arteriosclerosis - etiology Atherosclerotic plaque Biological and medical sciences Cholesterol Cholesterol, HDL - blood Cholesterol, HDL - drug effects Cholesterol, LDL - blood Cholesterol, LDL - drug effects Disease Models, Animal Endothelial dysfunction Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism General and cellular metabolism. Vitamins HMG-CoA reductase inhibitor Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Hypercholesterolemia - blood Hypercholesterolemia - drug therapy Hypercholesterolemia - etiology LDLR-knockout Male Medical sciences Mice Mice, Knockout Models, Cardiovascular Mouse Muscle Relaxation - drug effects Nitric Oxide - biosynthesis Nitric Oxide Synthase - biosynthesis Nitric Oxide Synthase - drug effects Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III NOS-3 Pharmacology. Drug treatments Receptors, LDL - deficiency Receptors, LDL - drug effects RNA, Messenger - biosynthesis RNA, Messenger - drug effects Simvastatin - therapeutic use Treatment Outcome Triglycerides - blood Vasodilator Agents - pharmacology |
| title | Anti-atherosclerotic effect of simvastatin depends on the presence of apolipoprotein E |
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