Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E
Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and...
Gespeichert in:
| Veröffentlicht in: | PloS one 2008-06, Vol.3 (6), p.e2503-e2503 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e2503 |
|---|---|
| container_issue | 6 |
| container_start_page | e2503 |
| container_title | PloS one |
| container_volume | 3 |
| creator | Ma, Yanqing Malbon, Craig C Williams, David L Thorngate, Fayanne E |
| description | Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and atherosclerosis was tested further by suppression of aortic lesion formation in apoE(-/-) mice by expression of very low levels of transgenic apolipoprotein E.
We show that at 8.5 months of age, the apoE(-/-) mice display elevated expression of mRNA for LFA-1, MAC-1, VCAM-1, ICAM-1, and for CD44, as well as MCP-1, cathepsin B, and COX-2 (but not that for eNOS) in atherosclerotic aortic arches. At earlier age, (10-13 week old) apoE(-/-) mice already display elevated expression of mRNA of CD44, LFA-1, MAC-1, VCAM-1, ICAM-1, cathepsin, and of COX-2 in lesioned aortic arches. Expressing very low levels of transgenic apolipoprotein E suppresses both aortic lesions and the expression of mRNA of LFA-1, VCAM-1, MCP-1, cathepsin B, and of ICAM-1 in ApoE(-/-) mice. We tested at the level of protein, the observations obtained for mRNA expression. CD11a (a component of LFA-1), VCAM-1 and cathepsin B expression was found to be elevated in apoE(-/-) aortas at 8-9 months; low level expression of transgenic apolipoprotein E rectifies these changes.
Atherosclerotic lesions in apoE(-/-) mice are detected as early as 4 weeks of age. Expression of low levels of apoE is shown to be both atheroprotective and to suppress these changes in key adhesion and inflammatory molecules observed in early atherosclerotic lesions. |
| doi_str_mv | 10.1371/journal.pone.0002503 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1312291076</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A472647524</galeid><doaj_id>oai_doaj_org_article_310ba749fe6b44a083bf4870d55fa14c</doaj_id><sourcerecordid>A472647524</sourcerecordid><originalsourceid>FETCH-LOGICAL-c759t-8b5a2264893ff4979a25f29abb0d2ba030ee9ca4d21f946f1a11f8eaf78c562d3</originalsourceid><addsrcrecordid>eNqNk12L1DAUhoso7rr6D0QLwoIXM-araXMjDMuqAwsLfoFX4bQ9mcmYabpJu-78ezPOqDMiKA1NSZ73bc7JOVn2lJIp5SV9tfJj6MBNe9_hlBDCCsLvZadUcTaRjPD7B98n2aMYV4QUvJLyYXZCq0KSQorT7MvMDRiwzRfYYY53fcAYre9y2-UIwW1yGJYYfGzc9m1jnkbtfPM1aepN7vy33OEtuhx672zv--AHTOLLx9kDAy7ik_18ln16c_nx4t3k6vrt_GJ2NWnKQg2Tqi6AMSkqxY0RqlTACsMU1DVpWQ2EE0TVgGgZNUpIQ4FSUyGYsmoKyVp-lj3f-fbOR73PStSUU8YUJaVMxHxHtB5Wug92DWGjPVj9Y8GHhYYw2BSh5pTUUAplUNZCAKl4bURVkrYoDFDRJK_X-7-N9RrbBrshgDsyPd7p7FIv_K1mgnFRiWRwvjcI_mbEOOi1jQ06Bx36MWqpGCtpJf8JUlXSQlUsgS_-AP-ehOmOWkCK03bGp-M16WlxbZtUQ8am9Zko012UBdse9OWRIDED3g0LGGPU8w_v_5-9_nzMnh-wSwQ3LKN345CqLh6DYgc2qfBiQPMry5TobQv8jFNvW0DvWyDJnh3e0G_Rvub5d-KCAnY</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1312291076</pqid></control><display><type>article</type><title>Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E</title><source>Public Library of Science (PLoS) Journals Open Access</source><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Ma, Yanqing ; Malbon, Craig C ; Williams, David L ; Thorngate, Fayanne E</creator><contributor>Pockley, Graham</contributor><creatorcontrib>Ma, Yanqing ; Malbon, Craig C ; Williams, David L ; Thorngate, Fayanne E ; Pockley, Graham</creatorcontrib><description>Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and atherosclerosis was tested further by suppression of aortic lesion formation in apoE(-/-) mice by expression of very low levels of transgenic apolipoprotein E.
We show that at 8.5 months of age, the apoE(-/-) mice display elevated expression of mRNA for LFA-1, MAC-1, VCAM-1, ICAM-1, and for CD44, as well as MCP-1, cathepsin B, and COX-2 (but not that for eNOS) in atherosclerotic aortic arches. At earlier age, (10-13 week old) apoE(-/-) mice already display elevated expression of mRNA of CD44, LFA-1, MAC-1, VCAM-1, ICAM-1, cathepsin, and of COX-2 in lesioned aortic arches. Expressing very low levels of transgenic apolipoprotein E suppresses both aortic lesions and the expression of mRNA of LFA-1, VCAM-1, MCP-1, cathepsin B, and of ICAM-1 in ApoE(-/-) mice. We tested at the level of protein, the observations obtained for mRNA expression. CD11a (a component of LFA-1), VCAM-1 and cathepsin B expression was found to be elevated in apoE(-/-) aortas at 8-9 months; low level expression of transgenic apolipoprotein E rectifies these changes.
Atherosclerotic lesions in apoE(-/-) mice are detected as early as 4 weeks of age. Expression of low levels of apoE is shown to be both atheroprotective and to suppress these changes in key adhesion and inflammatory molecules observed in early atherosclerotic lesions.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0002503</identifier><identifier>PMID: 18560564</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adhesion ; Adhesion tests ; Age ; Animals ; Aorta ; Aorta - metabolism ; Apolipoprotein E ; Apolipoproteins ; Apolipoproteins E - blood ; Apolipoproteins E - genetics ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - genetics ; Base Sequence ; Blotting, Western ; Bone marrow ; Cardiovascular disease ; Cardiovascular Disorders ; Cardiovascular Disorders/Vascular Biology ; Cathepsin B ; Cathepsins ; CD11a antigen ; CD44 antigen ; Cell adhesion & migration ; Cell Biology/Cell Adhesion ; Cell Biology/Gene Expression ; Chemokines ; Cofactors ; Cyclooxygenase-2 ; Development and progression ; DNA Primers ; Gene Expression ; Genetic aspects ; Genetic engineering ; Growth factors ; Immunohistochemistry ; Inflammation ; Intercellular adhesion molecule 1 ; Lesions ; LFA-1 antigen ; Ligands ; Lipids ; Low level ; Lymphocyte Function-Associated Antigen-1 - metabolism ; Mac1 protein ; Medicine ; Metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Monocyte chemoattractant protein 1 ; Phosphorylation ; Proteins ; RNA ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Signal transduction ; Smooth muscle ; Studies ; Transgenic animals ; Vascular cell adhesion molecule 1 ; Vascular Cell Adhesion Molecule-1 - metabolism</subject><ispartof>PloS one, 2008-06, Vol.3 (6), p.e2503-e2503</ispartof><rights>COPYRIGHT 2008 Public Library of Science</rights><rights>2008 Ma et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Ma et al. 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c759t-8b5a2264893ff4979a25f29abb0d2ba030ee9ca4d21f946f1a11f8eaf78c562d3</citedby><cites>FETCH-LOGICAL-c759t-8b5a2264893ff4979a25f29abb0d2ba030ee9ca4d21f946f1a11f8eaf78c562d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2423484/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2423484/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18560564$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Pockley, Graham</contributor><creatorcontrib>Ma, Yanqing</creatorcontrib><creatorcontrib>Malbon, Craig C</creatorcontrib><creatorcontrib>Williams, David L</creatorcontrib><creatorcontrib>Thorngate, Fayanne E</creatorcontrib><title>Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and atherosclerosis was tested further by suppression of aortic lesion formation in apoE(-/-) mice by expression of very low levels of transgenic apolipoprotein E.
We show that at 8.5 months of age, the apoE(-/-) mice display elevated expression of mRNA for LFA-1, MAC-1, VCAM-1, ICAM-1, and for CD44, as well as MCP-1, cathepsin B, and COX-2 (but not that for eNOS) in atherosclerotic aortic arches. At earlier age, (10-13 week old) apoE(-/-) mice already display elevated expression of mRNA of CD44, LFA-1, MAC-1, VCAM-1, ICAM-1, cathepsin, and of COX-2 in lesioned aortic arches. Expressing very low levels of transgenic apolipoprotein E suppresses both aortic lesions and the expression of mRNA of LFA-1, VCAM-1, MCP-1, cathepsin B, and of ICAM-1 in ApoE(-/-) mice. We tested at the level of protein, the observations obtained for mRNA expression. CD11a (a component of LFA-1), VCAM-1 and cathepsin B expression was found to be elevated in apoE(-/-) aortas at 8-9 months; low level expression of transgenic apolipoprotein E rectifies these changes.
Atherosclerotic lesions in apoE(-/-) mice are detected as early as 4 weeks of age. Expression of low levels of apoE is shown to be both atheroprotective and to suppress these changes in key adhesion and inflammatory molecules observed in early atherosclerotic lesions.</description><subject>Adhesion</subject><subject>Adhesion tests</subject><subject>Age</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta - metabolism</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins</subject><subject>Apolipoproteins E - blood</subject><subject>Apolipoproteins E - genetics</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - genetics</subject><subject>Base Sequence</subject><subject>Blotting, Western</subject><subject>Bone marrow</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular Disorders</subject><subject>Cardiovascular Disorders/Vascular Biology</subject><subject>Cathepsin B</subject><subject>Cathepsins</subject><subject>CD11a antigen</subject><subject>CD44 antigen</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology/Cell Adhesion</subject><subject>Cell Biology/Gene Expression</subject><subject>Chemokines</subject><subject>Cofactors</subject><subject>Cyclooxygenase-2</subject><subject>Development and progression</subject><subject>DNA Primers</subject><subject>Gene Expression</subject><subject>Genetic aspects</subject><subject>Genetic engineering</subject><subject>Growth factors</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Intercellular adhesion molecule 1</subject><subject>Lesions</subject><subject>LFA-1 antigen</subject><subject>Ligands</subject><subject>Lipids</subject><subject>Low level</subject><subject>Lymphocyte Function-Associated Antigen-1 - metabolism</subject><subject>Mac1 protein</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>RNA</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Smooth muscle</subject><subject>Studies</subject><subject>Transgenic animals</subject><subject>Vascular cell adhesion molecule 1</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7rr6D0QLwoIXM-araXMjDMuqAwsLfoFX4bQ9mcmYabpJu-78ezPOqDMiKA1NSZ73bc7JOVn2lJIp5SV9tfJj6MBNe9_hlBDCCsLvZadUcTaRjPD7B98n2aMYV4QUvJLyYXZCq0KSQorT7MvMDRiwzRfYYY53fcAYre9y2-UIwW1yGJYYfGzc9m1jnkbtfPM1aepN7vy33OEtuhx672zv--AHTOLLx9kDAy7ik_18ln16c_nx4t3k6vrt_GJ2NWnKQg2Tqi6AMSkqxY0RqlTACsMU1DVpWQ2EE0TVgGgZNUpIQ4FSUyGYsmoKyVp-lj3f-fbOR73PStSUU8YUJaVMxHxHtB5Wug92DWGjPVj9Y8GHhYYw2BSh5pTUUAplUNZCAKl4bURVkrYoDFDRJK_X-7-N9RrbBrshgDsyPd7p7FIv_K1mgnFRiWRwvjcI_mbEOOi1jQ06Bx36MWqpGCtpJf8JUlXSQlUsgS_-AP-ehOmOWkCK03bGp-M16WlxbZtUQ8am9Zko012UBdse9OWRIDED3g0LGGPU8w_v_5-9_nzMnh-wSwQ3LKN345CqLh6DYgc2qfBiQPMry5TobQv8jFNvW0DvWyDJnh3e0G_Rvub5d-KCAnY</recordid><startdate>20080618</startdate><enddate>20080618</enddate><creator>Ma, Yanqing</creator><creator>Malbon, Craig C</creator><creator>Williams, David L</creator><creator>Thorngate, Fayanne E</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20080618</creationdate><title>Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E</title><author>Ma, Yanqing ; Malbon, Craig C ; Williams, David L ; Thorngate, Fayanne E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c759t-8b5a2264893ff4979a25f29abb0d2ba030ee9ca4d21f946f1a11f8eaf78c562d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adhesion</topic><topic>Adhesion tests</topic><topic>Age</topic><topic>Animals</topic><topic>Aorta</topic><topic>Aorta - metabolism</topic><topic>Apolipoprotein E</topic><topic>Apolipoproteins</topic><topic>Apolipoproteins E - blood</topic><topic>Apolipoproteins E - genetics</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - genetics</topic><topic>Base Sequence</topic><topic>Blotting, Western</topic><topic>Bone marrow</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular Disorders</topic><topic>Cardiovascular Disorders/Vascular Biology</topic><topic>Cathepsin B</topic><topic>Cathepsins</topic><topic>CD11a antigen</topic><topic>CD44 antigen</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology/Cell Adhesion</topic><topic>Cell Biology/Gene Expression</topic><topic>Chemokines</topic><topic>Cofactors</topic><topic>Cyclooxygenase-2</topic><topic>Development and progression</topic><topic>DNA Primers</topic><topic>Gene Expression</topic><topic>Genetic aspects</topic><topic>Genetic engineering</topic><topic>Growth factors</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Intercellular adhesion molecule 1</topic><topic>Lesions</topic><topic>LFA-1 antigen</topic><topic>Ligands</topic><topic>Lipids</topic><topic>Low level</topic><topic>Lymphocyte Function-Associated Antigen-1 - metabolism</topic><topic>Mac1 protein</topic><topic>Medicine</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>RNA</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Smooth muscle</topic><topic>Studies</topic><topic>Transgenic animals</topic><topic>Vascular cell adhesion molecule 1</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Yanqing</creatorcontrib><creatorcontrib>Malbon, Craig C</creatorcontrib><creatorcontrib>Williams, David L</creatorcontrib><creatorcontrib>Thorngate, Fayanne E</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Yanqing</au><au>Malbon, Craig C</au><au>Williams, David L</au><au>Thorngate, Fayanne E</au><au>Pockley, Graham</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2008-06-18</date><risdate>2008</risdate><volume>3</volume><issue>6</issue><spage>e2503</spage><epage>e2503</epage><pages>e2503-e2503</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Mice deficient in apolipoprotein E (apoE(-/-)) develop atherosclerosis. The possible linkage between expression of adhesion molecules/cofactors and atherosclerosis was probed at the level of mRNA and protein expression. The hypothesis of a linkage between changes of adhesion molecules/cofactors and atherosclerosis was tested further by suppression of aortic lesion formation in apoE(-/-) mice by expression of very low levels of transgenic apolipoprotein E.
We show that at 8.5 months of age, the apoE(-/-) mice display elevated expression of mRNA for LFA-1, MAC-1, VCAM-1, ICAM-1, and for CD44, as well as MCP-1, cathepsin B, and COX-2 (but not that for eNOS) in atherosclerotic aortic arches. At earlier age, (10-13 week old) apoE(-/-) mice already display elevated expression of mRNA of CD44, LFA-1, MAC-1, VCAM-1, ICAM-1, cathepsin, and of COX-2 in lesioned aortic arches. Expressing very low levels of transgenic apolipoprotein E suppresses both aortic lesions and the expression of mRNA of LFA-1, VCAM-1, MCP-1, cathepsin B, and of ICAM-1 in ApoE(-/-) mice. We tested at the level of protein, the observations obtained for mRNA expression. CD11a (a component of LFA-1), VCAM-1 and cathepsin B expression was found to be elevated in apoE(-/-) aortas at 8-9 months; low level expression of transgenic apolipoprotein E rectifies these changes.
Atherosclerotic lesions in apoE(-/-) mice are detected as early as 4 weeks of age. Expression of low levels of apoE is shown to be both atheroprotective and to suppress these changes in key adhesion and inflammatory molecules observed in early atherosclerotic lesions.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>18560564</pmid><doi>10.1371/journal.pone.0002503</doi><tpages>e2503</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2008-06, Vol.3 (6), p.e2503-e2503 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1312291076 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adhesion Adhesion tests Age Animals Aorta Aorta - metabolism Apolipoprotein E Apolipoproteins Apolipoproteins E - blood Apolipoproteins E - genetics Arteriosclerosis Atherosclerosis Atherosclerosis - genetics Base Sequence Blotting, Western Bone marrow Cardiovascular disease Cardiovascular Disorders Cardiovascular Disorders/Vascular Biology Cathepsin B Cathepsins CD11a antigen CD44 antigen Cell adhesion & migration Cell Biology/Cell Adhesion Cell Biology/Gene Expression Chemokines Cofactors Cyclooxygenase-2 Development and progression DNA Primers Gene Expression Genetic aspects Genetic engineering Growth factors Immunohistochemistry Inflammation Intercellular adhesion molecule 1 Lesions LFA-1 antigen Ligands Lipids Low level Lymphocyte Function-Associated Antigen-1 - metabolism Mac1 protein Medicine Metabolism Mice Mice, Knockout Mice, Transgenic Monocyte chemoattractant protein 1 Phosphorylation Proteins RNA RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Signal transduction Smooth muscle Studies Transgenic animals Vascular cell adhesion molecule 1 Vascular Cell Adhesion Molecule-1 - metabolism |
| title | Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T15%3A57%3A00IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Altered%20gene%20expression%20in%20early%20atherosclerosis%20is%20blocked%20by%20low%20level%20apolipoprotein%20E&rft.jtitle=PloS%20one&rft.au=Ma,%20Yanqing&rft.date=2008-06-18&rft.volume=3&rft.issue=6&rft.spage=e2503&rft.epage=e2503&rft.pages=e2503-e2503&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0002503&rft_dat=%3Cgale_plos_%3EA472647524%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1312291076&rft_id=info:pmid/18560564&rft_galeid=A472647524&rft_doaj_id=oai_doaj_org_article_310ba749fe6b44a083bf4870d55fa14c&rfr_iscdi=true |