Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice
Macrophage internalization of modified lipoproteins is thought to play a critical role in the initiation of atherogenesis. Two scavenger receptors, scavenger receptor A (SR-A) and CD36, have been centrally implicated in this lipid uptake process. Previous studies showed that these receptors mediated...
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| Veröffentlicht in: | The Journal of clinical investigation 2005-08, Vol.115 (8), p.2192-2201 |
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| creator | Moore, Kathryn J Kunjathoor, Vidya V Koehn, Stephanie L Manning, Jennifer J Tseng, Anita A Silver, Jessica M McKee, Mary Freeman, Mason W |
| description | Macrophage internalization of modified lipoproteins is thought to play a critical role in the initiation of atherogenesis. Two scavenger receptors, scavenger receptor A (SR-A) and CD36, have been centrally implicated in this lipid uptake process. Previous studies showed that these receptors mediated the majority of cholesterol ester accumulation in macrophages exposed to oxidized LDL and that mice with deletions of either receptor exhibited marked reductions in atherosclerosis. This work has contributed to an atherosclerosis paradigm: scavenger receptor-mediated oxidized lipoprotein uptake is required for foam cell formation and atherogenesis. In this study, Apoe-/- mice lacking SR-A or CD36, backcrossed into the C57BL/6 strain for 7 generations, were fed an atherogenic diet for 8 weeks. Hyperlipidemic Cd36-/-Apoe-/- and Msr1-/-Apoe-/- mice showed significant reductions in peritoneal macrophage lipid accumulation in vivo; however, in contrast with previous reports, this was associated with increased aortic sinus lesion areas. Characterization of aortic sinus lesions by electron microscopy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by intimal macrophages occurs in the absence of CD36 or SR-A. These data show that alternative lipid uptake mechanisms may contribute to macrophage cholesterol ester accumulation in vivo and suggest that the roles of SR-A and CD36 as proatherosclerotic mediators of modified LDL uptake in vivo need to be reassessed. |
| doi_str_mv | 10.1172/JCI24061 |
| format | Article |
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Two scavenger receptors, scavenger receptor A (SR-A) and CD36, have been centrally implicated in this lipid uptake process. Previous studies showed that these receptors mediated the majority of cholesterol ester accumulation in macrophages exposed to oxidized LDL and that mice with deletions of either receptor exhibited marked reductions in atherosclerosis. This work has contributed to an atherosclerosis paradigm: scavenger receptor-mediated oxidized lipoprotein uptake is required for foam cell formation and atherogenesis. In this study, Apoe-/- mice lacking SR-A or CD36, backcrossed into the C57BL/6 strain for 7 generations, were fed an atherogenic diet for 8 weeks. Hyperlipidemic Cd36-/-Apoe-/- and Msr1-/-Apoe-/- mice showed significant reductions in peritoneal macrophage lipid accumulation in vivo; however, in contrast with previous reports, this was associated with increased aortic sinus lesion areas. Characterization of aortic sinus lesions by electron microscopy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by intimal macrophages occurs in the absence of CD36 or SR-A. These data show that alternative lipid uptake mechanisms may contribute to macrophage cholesterol ester accumulation in vivo and suggest that the roles of SR-A and CD36 as proatherosclerotic mediators of modified LDL uptake in vivo need to be reassessed.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/JCI24061</identifier><identifier>PMID: 16075060</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Animals ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Arteriosclerosis - genetics ; Arteriosclerosis - metabolism ; Arteriosclerosis - pathology ; Atherosclerosis ; Biomedical research ; CD36 Antigens - genetics ; CD36 Antigens - metabolism ; Cholesterol ; Cholesterol Esters - metabolism ; Chromatography ; Diet, Atherogenic ; Foam Cells - metabolism ; Foam Cells - pathology ; Hyperlipidemias - genetics ; Hyperlipidemias - metabolism ; Hyperlipidemias - pathology ; Hypotheses ; Lipids ; Lipoproteins ; Lipoproteins, LDL - metabolism ; Macrophages, Peritoneal - metabolism ; Macrophages, Peritoneal - pathology ; Mice ; Mice, Knockout ; Oxidation ; Receptors, Immunologic - genetics ; Receptors, Immunologic - metabolism ; Receptors, Scavenger ; Scavenger Receptors, Class A ; Sinus of Valsalva - metabolism ; Sinus of Valsalva - pathology ; Sinuses</subject><ispartof>The Journal of clinical investigation, 2005-08, Vol.115 (8), p.2192-2201</ispartof><rights>Copyright American Society for Clinical Investigation Aug 2005</rights><rights>Copyright © 2005, American Society for Clinical Investigation 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-a6b7b7eb21891e4ac2cc0746debe55f4110adcca21868cdc6bd765cc81bca1653</citedby><cites>FETCH-LOGICAL-c436t-a6b7b7eb21891e4ac2cc0746debe55f4110adcca21868cdc6bd765cc81bca1653</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/PMC1180534/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1180534/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16075060$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moore, Kathryn J</creatorcontrib><creatorcontrib>Kunjathoor, Vidya V</creatorcontrib><creatorcontrib>Koehn, Stephanie L</creatorcontrib><creatorcontrib>Manning, Jennifer J</creatorcontrib><creatorcontrib>Tseng, Anita A</creatorcontrib><creatorcontrib>Silver, Jessica M</creatorcontrib><creatorcontrib>McKee, Mary</creatorcontrib><creatorcontrib>Freeman, Mason W</creatorcontrib><title>Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Macrophage internalization of modified lipoproteins is thought to play a critical role in the initiation of atherogenesis. Two scavenger receptors, scavenger receptor A (SR-A) and CD36, have been centrally implicated in this lipid uptake process. Previous studies showed that these receptors mediated the majority of cholesterol ester accumulation in macrophages exposed to oxidized LDL and that mice with deletions of either receptor exhibited marked reductions in atherosclerosis. This work has contributed to an atherosclerosis paradigm: scavenger receptor-mediated oxidized lipoprotein uptake is required for foam cell formation and atherogenesis. In this study, Apoe-/- mice lacking SR-A or CD36, backcrossed into the C57BL/6 strain for 7 generations, were fed an atherogenic diet for 8 weeks. Hyperlipidemic Cd36-/-Apoe-/- and Msr1-/-Apoe-/- mice showed significant reductions in peritoneal macrophage lipid accumulation in vivo; however, in contrast with previous reports, this was associated with increased aortic sinus lesion areas. Characterization of aortic sinus lesions by electron microscopy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by intimal macrophages occurs in the absence of CD36 or SR-A. These data show that alternative lipid uptake mechanisms may contribute to macrophage cholesterol ester accumulation in vivo and suggest that the roles of SR-A and CD36 as proatherosclerotic mediators of modified LDL uptake in vivo need to be reassessed.</description><subject>Animals</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Arteriosclerosis - genetics</subject><subject>Arteriosclerosis - metabolism</subject><subject>Arteriosclerosis - pathology</subject><subject>Atherosclerosis</subject><subject>Biomedical research</subject><subject>CD36 Antigens - genetics</subject><subject>CD36 Antigens - metabolism</subject><subject>Cholesterol</subject><subject>Cholesterol Esters - metabolism</subject><subject>Chromatography</subject><subject>Diet, Atherogenic</subject><subject>Foam Cells - metabolism</subject><subject>Foam Cells - pathology</subject><subject>Hyperlipidemias - genetics</subject><subject>Hyperlipidemias - metabolism</subject><subject>Hyperlipidemias - pathology</subject><subject>Hypotheses</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Macrophages, Peritoneal - pathology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Oxidation</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Receptors, Scavenger</subject><subject>Scavenger Receptors, Class A</subject><subject>Sinus of Valsalva - metabolism</subject><subject>Sinus of Valsalva - pathology</subject><subject>Sinuses</subject><issn>0021-9738</issn><issn>1558-8238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc1u1DAUhS0EokNB4gmQxaLqJuCb2I5ng1QNhbYaiQ2sLefmTscliYOdDJpn6Evj0qFAF75enE_n_hzGXoN4B1CX769Wl6UUGp6wBShlClNW5ilbCFFCsawrc8RepHQjBEip5HN2BFrUSmixYLfrkBIPGx4JaZxCLHpqvZuo5Z0ffcvncXLfie-84wndjoZrig8wP-O5rD5Wmo9u2v50-8TbQIkPYeKup86HmL141iiGhN1d9Yn7gW_3I8XfLaj3yPOjl-zZxnWJXh3-Y_bt0_nX1UWx_vL5cnW2LlBWeiqcbuqmpqYEswSSDktEUUvdUkNKbSSAcC2iy7o22KJu2lorRAMNOtCqOmYf7n3HucnbIg1TdJ0do-9d3NvgvP1fGfzWXoedBTBCVTIbnBwMYvgxU5ps7xNS17mBwpysNlIKqSCDbx-BN2GOQ17OlkKoUi3VMkOn9xDm46RIm4dJQNi7eO2feDP65t_J_4KHPKtf5TWjaw</recordid><startdate>200508</startdate><enddate>200508</enddate><creator>Moore, Kathryn J</creator><creator>Kunjathoor, Vidya V</creator><creator>Koehn, Stephanie L</creator><creator>Manning, Jennifer J</creator><creator>Tseng, Anita A</creator><creator>Silver, Jessica M</creator><creator>McKee, Mary</creator><creator>Freeman, Mason W</creator><general>American Society for Clinical Investigation</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200508</creationdate><title>Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice</title><author>Moore, Kathryn J ; Kunjathoor, Vidya V ; Koehn, Stephanie L ; Manning, Jennifer J ; Tseng, Anita A ; Silver, Jessica M ; McKee, Mary ; Freeman, Mason W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-a6b7b7eb21891e4ac2cc0746debe55f4110adcca21868cdc6bd765cc81bca1653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apolipoproteins E - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moore, Kathryn J</au><au>Kunjathoor, Vidya V</au><au>Koehn, Stephanie L</au><au>Manning, Jennifer J</au><au>Tseng, Anita A</au><au>Silver, Jessica M</au><au>McKee, Mary</au><au>Freeman, Mason W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>2005-08</date><risdate>2005</risdate><volume>115</volume><issue>8</issue><spage>2192</spage><epage>2201</epage><pages>2192-2201</pages><issn>0021-9738</issn><eissn>1558-8238</eissn><abstract>Macrophage internalization of modified lipoproteins is thought to play a critical role in the initiation of atherogenesis. Two scavenger receptors, scavenger receptor A (SR-A) and CD36, have been centrally implicated in this lipid uptake process. Previous studies showed that these receptors mediated the majority of cholesterol ester accumulation in macrophages exposed to oxidized LDL and that mice with deletions of either receptor exhibited marked reductions in atherosclerosis. This work has contributed to an atherosclerosis paradigm: scavenger receptor-mediated oxidized lipoprotein uptake is required for foam cell formation and atherogenesis. In this study, Apoe-/- mice lacking SR-A or CD36, backcrossed into the C57BL/6 strain for 7 generations, were fed an atherogenic diet for 8 weeks. Hyperlipidemic Cd36-/-Apoe-/- and Msr1-/-Apoe-/- mice showed significant reductions in peritoneal macrophage lipid accumulation in vivo; however, in contrast with previous reports, this was associated with increased aortic sinus lesion areas. Characterization of aortic sinus lesions by electron microscopy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by intimal macrophages occurs in the absence of CD36 or SR-A. These data show that alternative lipid uptake mechanisms may contribute to macrophage cholesterol ester accumulation in vivo and suggest that the roles of SR-A and CD36 as proatherosclerotic mediators of modified LDL uptake in vivo need to be reassessed.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>16075060</pmid><doi>10.1172/JCI24061</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Apolipoproteins E - genetics Apolipoproteins E - metabolism Arteriosclerosis - genetics Arteriosclerosis - metabolism Arteriosclerosis - pathology Atherosclerosis Biomedical research CD36 Antigens - genetics CD36 Antigens - metabolism Cholesterol Cholesterol Esters - metabolism Chromatography Diet, Atherogenic Foam Cells - metabolism Foam Cells - pathology Hyperlipidemias - genetics Hyperlipidemias - metabolism Hyperlipidemias - pathology Hypotheses Lipids Lipoproteins Lipoproteins, LDL - metabolism Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - pathology Mice Mice, Knockout Oxidation Receptors, Immunologic - genetics Receptors, Immunologic - metabolism Receptors, Scavenger Scavenger Receptors, Class A Sinus of Valsalva - metabolism Sinus of Valsalva - pathology Sinuses |
| title | Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice |
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