Retinoic acid induces macrophage cholesterol efflux and inhibits atherosclerotic plaque formation in apoE-deficient mice
It has been suggested that retinoic acid (RA) has a potential role in the prevention of atherosclerotic CVD. In the present study, we used J774A.1 cell lines and primary peritoneal macrophages to investigate the protective effects of RA on foam cell formation and atherogenesis in apoE-deficient (apo...
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| Veröffentlicht in: | British journal of nutrition 2015-08, Vol.114 (4), p.509-518 |
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| creator | Zhou, Wenjing Lin, Jiacheng Chen, Hongen Wang, Jingjing Liu, Yan Xia, Min |
| description | It has been suggested that retinoic acid (RA) has a potential role in the prevention of atherosclerotic CVD. In the present study, we used J774A.1 cell lines and primary peritoneal macrophages to investigate the protective effects of RA on foam cell formation and atherogenesis in apoE-deficient (apoE− / −) mice. A total of twenty male apoE− / − mice (n 10 animals per group), aged 8 weeks, were fed on a high-fat diet (HFD) and treated with vehicle or 9-cis-RA for 8 weeks. The atherosclerotic plaque area in the aortic sinus of mice in the 9-cis-RA group was 40·7 % less than that of mice in the control group (P |
| doi_str_mv | 10.1017/S0007114515002159 |
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In the present study, we used J774A.1 cell lines and primary peritoneal macrophages to investigate the protective effects of RA on foam cell formation and atherogenesis in apoE-deficient (apoE− / −) mice. A total of twenty male apoE− / − mice (n 10 animals per group), aged 8 weeks, were fed on a high-fat diet (HFD) and treated with vehicle or 9-cis-RA for 8 weeks. The atherosclerotic plaque area in the aortic sinus of mice in the 9-cis-RA group was 40·7 % less than that of mice in the control group (P< 0·01). Mouse peritoneal macrophages from the 9-cis-RA group had higher protein expression levels of ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) than those from the control group. Serum total and LDL-cholesterol concentrations were lower in the 9-cis-RA group than in the control group (P< 0·05). In vitro studies showed that incubation of cholesterol-loaded J774A.1 macrophages with 9-cis-RA (0·1, 1 and 10 μmol/l) induced cholesterol efflux in a dose-dependent manner. The 9-cis-RA treatment markedly attenuated lipid accumulation in macrophages exposed to oxidised LDL. Moreover, treatment with 9-cis-RA significantly increased the protein expression levels of ABCA1 and ABCG1 in J774A.1 macrophages in a dose-dependent manner. Furthermore, 9-cis-RA dose-dependently enhanced the protein expression level of liver X receptor-α (LXRα), the upstream regulator of ABCA1 and ABCG1. Taken together, the present results show that 9-cis-RA suppresses foam cell formation and prevents HFD-induced atherogenesis via the LXRα-dependent up-regulation of ABCA1 and ABCG1.</description><identifier>ISSN: 0007-1145</identifier><identifier>EISSN: 1475-2662</identifier><identifier>DOI: 10.1017/S0007114515002159</identifier><identifier>PMID: 26201974</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Animals ; Aorta ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Atherosclerosis ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Atherosclerosis - prevention & control ; ATP Binding Cassette Transporter 1 - metabolism ; Cell Line ; Cholesterol ; Cholesterol - metabolism ; Cholesterol, LDL - blood ; Diet, High-Fat ; Foam Cells - metabolism ; Lipoproteins, LDL - metabolism ; Liver X Receptors ; Macrophages, Peritoneal - drug effects ; Macrophages, Peritoneal - metabolism ; Male ; Mice, Knockout ; Molecular Nutrition ; Orphan Nuclear Receptors - metabolism ; Plaque, Atherosclerotic - metabolism ; Plaque, Atherosclerotic - prevention & control ; Rodents ; Tretinoin - pharmacology ; Tretinoin - therapeutic use ; Up-Regulation ; Vitamin A</subject><ispartof>British journal of nutrition, 2015-08, Vol.114 (4), p.509-518</ispartof><rights>Copyright © The Authors 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c515t-3286c9c49f839d13cff3f747cc6a12dfd1dc8d2a6e0cdb76de78163c4ff7772f3</citedby><cites>FETCH-LOGICAL-c515t-3286c9c49f839d13cff3f747cc6a12dfd1dc8d2a6e0cdb76de78163c4ff7772f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0007114515002159/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>164,314,776,780,27903,27904,55607</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26201974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Wenjing</creatorcontrib><creatorcontrib>Lin, Jiacheng</creatorcontrib><creatorcontrib>Chen, Hongen</creatorcontrib><creatorcontrib>Wang, Jingjing</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><creatorcontrib>Xia, Min</creatorcontrib><title>Retinoic acid induces macrophage cholesterol efflux and inhibits atherosclerotic plaque formation in apoE-deficient mice</title><title>British journal of nutrition</title><addtitle>Br J Nutr</addtitle><description>It has been suggested that retinoic acid (RA) has a potential role in the prevention of atherosclerotic CVD. In the present study, we used J774A.1 cell lines and primary peritoneal macrophages to investigate the protective effects of RA on foam cell formation and atherogenesis in apoE-deficient (apoE− / −) mice. A total of twenty male apoE− / − mice (n 10 animals per group), aged 8 weeks, were fed on a high-fat diet (HFD) and treated with vehicle or 9-cis-RA for 8 weeks. The atherosclerotic plaque area in the aortic sinus of mice in the 9-cis-RA group was 40·7 % less than that of mice in the control group (P< 0·01). Mouse peritoneal macrophages from the 9-cis-RA group had higher protein expression levels of ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) than those from the control group. Serum total and LDL-cholesterol concentrations were lower in the 9-cis-RA group than in the control group (P< 0·05). In vitro studies showed that incubation of cholesterol-loaded J774A.1 macrophages with 9-cis-RA (0·1, 1 and 10 μmol/l) induced cholesterol efflux in a dose-dependent manner. The 9-cis-RA treatment markedly attenuated lipid accumulation in macrophages exposed to oxidised LDL. Moreover, treatment with 9-cis-RA significantly increased the protein expression levels of ABCA1 and ABCG1 in J774A.1 macrophages in a dose-dependent manner. Furthermore, 9-cis-RA dose-dependently enhanced the protein expression level of liver X receptor-α (LXRα), the upstream regulator of ABCA1 and ABCG1. Taken together, the present results show that 9-cis-RA suppresses foam cell formation and prevents HFD-induced atherogenesis via the LXRα-dependent up-regulation of ABCA1 and ABCG1.</description><subject>Animals</subject><subject>Aorta</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>Atherosclerosis - prevention & control</subject><subject>ATP Binding Cassette Transporter 1 - metabolism</subject><subject>Cell Line</subject><subject>Cholesterol</subject><subject>Cholesterol - metabolism</subject><subject>Cholesterol, LDL - blood</subject><subject>Diet, High-Fat</subject><subject>Foam Cells - metabolism</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Liver X Receptors</subject><subject>Macrophages, Peritoneal - drug effects</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Male</subject><subject>Mice, Knockout</subject><subject>Molecular Nutrition</subject><subject>Orphan Nuclear Receptors - metabolism</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Plaque, Atherosclerotic - prevention & control</subject><subject>Rodents</subject><subject>Tretinoin - pharmacology</subject><subject>Tretinoin - therapeutic use</subject><subject>Up-Regulation</subject><subject>Vitamin A</subject><issn>0007-1145</issn><issn>1475-2662</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkUuLFTEQhYMoznX0B7iRgBs3ramkb9K9lGF8wIDgY93kVipzM3R32iQNM__eNHMVUQQ3CeF8dSpVh7HnIF6DAPPmixDCALR72AshYd8_YDtozb6RWsuHbLfJzaafsSc539RnB6J_zM6klgJ60-7Y7WcqYY4BucXgeJjdipT5ZDHF5WivieMxjpQLpThy8n5cb7mdN_IYDqFkbsuxahnHepbqs4z2-0rcxzTZEuJcSW6XeNk48gEDzYVPAekpe-TtmOnZ6T5n395dfr340Fx9ev_x4u1Vg3Wq0ijZaeyx7X2negcKvVfetAZRW5DOO3DYOWk1CXQHox2ZDrTC1ntjjPTqnL26911SrP_KZZhCRhpHO1Nc8wCmdjBa6-4_UNFDB3XRFX35B3oT1zTXQTaqVX2rla4U3FN1mTkn8sOSwmTT3QBi2BIc_kqw1rw4Oa-Hidyvip-RVUCdTO10SMFd02-9_2n7A2z7pq0</recordid><startdate>20150828</startdate><enddate>20150828</enddate><creator>Zhou, Wenjing</creator><creator>Lin, Jiacheng</creator><creator>Chen, Hongen</creator><creator>Wang, Jingjing</creator><creator>Liu, Yan</creator><creator>Xia, Min</creator><general>Cambridge University Press</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>7QP</scope><scope>7RV</scope><scope>7T5</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20150828</creationdate><title>Retinoic acid induces macrophage cholesterol efflux and inhibits atherosclerotic plaque formation in apoE-deficient mice</title><author>Zhou, Wenjing ; Lin, Jiacheng ; Chen, Hongen ; Wang, Jingjing ; Liu, Yan ; Xia, Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-3286c9c49f839d13cff3f747cc6a12dfd1dc8d2a6e0cdb76de78163c4ff7772f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Aorta</topic><topic>Apolipoproteins E - genetics</topic><topic>Apolipoproteins E - metabolism</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>Atherosclerosis - prevention & control</topic><topic>ATP Binding Cassette Transporter 1 - metabolism</topic><topic>Cell Line</topic><topic>Cholesterol</topic><topic>Cholesterol - metabolism</topic><topic>Cholesterol, LDL - blood</topic><topic>Diet, High-Fat</topic><topic>Foam Cells - metabolism</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Liver X Receptors</topic><topic>Macrophages, Peritoneal - drug effects</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Male</topic><topic>Mice, Knockout</topic><topic>Molecular Nutrition</topic><topic>Orphan Nuclear Receptors - metabolism</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Plaque, Atherosclerotic - prevention & control</topic><topic>Rodents</topic><topic>Tretinoin - pharmacology</topic><topic>Tretinoin - therapeutic use</topic><topic>Up-Regulation</topic><topic>Vitamin A</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Wenjing</creatorcontrib><creatorcontrib>Lin, Jiacheng</creatorcontrib><creatorcontrib>Chen, Hongen</creatorcontrib><creatorcontrib>Wang, Jingjing</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><creatorcontrib>Xia, Min</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology 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>Public Health Database</collection><collection>ProQuest SciTech 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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Wenjing</au><au>Lin, Jiacheng</au><au>Chen, Hongen</au><au>Wang, Jingjing</au><au>Liu, Yan</au><au>Xia, Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Retinoic acid induces macrophage cholesterol efflux and inhibits atherosclerotic plaque formation in apoE-deficient mice</atitle><jtitle>British journal of nutrition</jtitle><addtitle>Br J Nutr</addtitle><date>2015-08-28</date><risdate>2015</risdate><volume>114</volume><issue>4</issue><spage>509</spage><epage>518</epage><pages>509-518</pages><issn>0007-1145</issn><eissn>1475-2662</eissn><abstract>It has been suggested that retinoic acid (RA) has a potential role in the prevention of atherosclerotic CVD. In the present study, we used J774A.1 cell lines and primary peritoneal macrophages to investigate the protective effects of RA on foam cell formation and atherogenesis in apoE-deficient (apoE− / −) mice. A total of twenty male apoE− / − mice (n 10 animals per group), aged 8 weeks, were fed on a high-fat diet (HFD) and treated with vehicle or 9-cis-RA for 8 weeks. The atherosclerotic plaque area in the aortic sinus of mice in the 9-cis-RA group was 40·7 % less than that of mice in the control group (P< 0·01). Mouse peritoneal macrophages from the 9-cis-RA group had higher protein expression levels of ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) than those from the control group. Serum total and LDL-cholesterol concentrations were lower in the 9-cis-RA group than in the control group (P< 0·05). In vitro studies showed that incubation of cholesterol-loaded J774A.1 macrophages with 9-cis-RA (0·1, 1 and 10 μmol/l) induced cholesterol efflux in a dose-dependent manner. The 9-cis-RA treatment markedly attenuated lipid accumulation in macrophages exposed to oxidised LDL. Moreover, treatment with 9-cis-RA significantly increased the protein expression levels of ABCA1 and ABCG1 in J774A.1 macrophages in a dose-dependent manner. Furthermore, 9-cis-RA dose-dependently enhanced the protein expression level of liver X receptor-α (LXRα), the upstream regulator of ABCA1 and ABCG1. Taken together, the present results show that 9-cis-RA suppresses foam cell formation and prevents HFD-induced atherogenesis via the LXRα-dependent up-regulation of ABCA1 and ABCG1.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>26201974</pmid><doi>10.1017/S0007114515002159</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Aorta Apolipoproteins E - genetics Apolipoproteins E - metabolism Atherosclerosis Atherosclerosis - metabolism Atherosclerosis - pathology Atherosclerosis - prevention & control ATP Binding Cassette Transporter 1 - metabolism Cell Line Cholesterol Cholesterol - metabolism Cholesterol, LDL - blood Diet, High-Fat Foam Cells - metabolism Lipoproteins, LDL - metabolism Liver X Receptors Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - metabolism Male Mice, Knockout Molecular Nutrition Orphan Nuclear Receptors - metabolism Plaque, Atherosclerotic - metabolism Plaque, Atherosclerotic - prevention & control Rodents Tretinoin - pharmacology Tretinoin - therapeutic use Up-Regulation Vitamin A |
| title | Retinoic acid induces macrophage cholesterol efflux and inhibits atherosclerotic plaque formation in apoE-deficient mice |
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