Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages

ATP-binding cassette transporters (ABC) A1 and G1 are key molecules in cholesterol efflux from macrophages, which is an initial step of reverse cholesterol transport (RCT), a major anti-atherogenic property of high-density lipoprotein (HDL). Astaxanthin is one of the naturally occurring carotenoids...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of Nutritional Science and Vitaminology 2012, Vol.58(2), pp.96-104
Hauptverfasser: IIZUKA, Maki, AYAORI, Makoto, UTO-KONDO, Harumi, YAKUSHIJI, Emi, TAKIGUCHI, Shunichi, NAKAYA, Kazuhiro, HISADA, Tetsuya, SASAKI, Makoto, KOMATSU, Tomohiro, YOGO, Makiko, KISHIMOTO, Yoshimi, KONDO, Kazuo, IKEWAKI, Katsunori
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 104
container_issue 2
container_start_page 96
container_title Journal of Nutritional Science and Vitaminology
container_volume 58
creator IIZUKA, Maki
AYAORI, Makoto
UTO-KONDO, Harumi
YAKUSHIJI, Emi
TAKIGUCHI, Shunichi
NAKAYA, Kazuhiro
HISADA, Tetsuya
SASAKI, Makoto
KOMATSU, Tomohiro
YOGO, Makiko
KISHIMOTO, Yoshimi
KONDO, Kazuo
IKEWAKI, Katsunori
description ATP-binding cassette transporters (ABC) A1 and G1 are key molecules in cholesterol efflux from macrophages, which is an initial step of reverse cholesterol transport (RCT), a major anti-atherogenic property of high-density lipoprotein (HDL). Astaxanthin is one of the naturally occurring carotenoids responsible for the pink-red pigmentation in a variety of living organisms. Although astaxanthin is known to be a strong antioxidant, it remains unclear through what mechanism of action it affects cholesterol homeostasis in macrophages. We therefore investigated the effects of astaxanthin on cholesterol efflux and ABCA1/G1 expressions in macrophages. Astaxanthin enhanced both apolipoprotein (apo) A-I- and HDL-mediated cholesterol efflux from RAW264.7 cells. In supporting these enhanced cholesterol efflux mechanisms, astaxanthin promoted ABCA1/G1 expression in various macrophages. In contrast, peroxisome proliferator-activated receptor γ, liver X receptor (LXR) α and LXRβ levels remained unchanged by astaxanthin. An experiment using actinomycin D demonstrated that astaxanthin transcriptionally induced ABCA1/G1 expression, and oxysterol depletion caused by overexpression of cholesterol sulfotransferase further revealed that these inductions in ABCA1/G1 were independent of LXR-mediated pathways. Finally, we performed luciferase assays using human ABCA1/G1 promoter-reporter constructs to reveal that astaxanthin activated both promoters irrespective of the presence or absence of LXR-responsive elements, indicating LXR-independence of these activations. In conclusion, astaxanthin increased ABCA1/G1 expression, thereby enhancing apoA-I/HDL-mediated cholesterol efflux from the macrophages in an LXR-independent manner. In addition to the anti-oxidative properties, the potential cardioprotective properties of astaxanthin might therefore be associated with an enhanced anti-atherogenic function of HDL.
doi_str_mv 10.3177/jnsv.58.96
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1372050821</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1372050821</sourcerecordid><originalsourceid>FETCH-LOGICAL-c581t-f9354216015eea8f9830ff6a751d5ddaf2210d91b02b8685578edd3e1d4212f13</originalsourceid><addsrcrecordid>eNpF0cuO0zAUBmALgZjOwIYHQN4gIaR0fIljZ8GiU5UBaRAsyjpy4-MmVWoHn3RU3h5XLWVlyf7ORb8JecfZXHKt73cBn-fKzOvqBZlxY3ihdSlekhmTjBelYeyG3CLuGCtrU5rX5EYIXTNV6RmJC5zs0Yap6wNdhc6GFpAu1j-Lhz64Pmzp0iLCNAFdJxtwjGmCRBf8_pHT1XFMgNjHgNQGR5ddHADzexzoyvvhcKQ-xT39btsUx85uAd-QV94OCG8v5x359WW1Xn4tnn48flsunopWGT4VvpaqFLxiXAFY42sjmfeV1Yo75Zz1QnDmar5hYmMqo5Q24JwE7nKV8FzekY_nvmOKvw95qWbfYwvDYAPEAzZcasEUM-JEP51pXhIxgW_G1O9t-tNw1pwCbk4BN8o0dZXx-0vfw2YP7kr_JZrBhwuw2NrB59DaHv-7ignGKpnd57Pb5Q_YwhXYNPXtANeZ4jz4et92NjUQ5F_o4Zql</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1372050821</pqid></control><display><type>article</type><title>Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages</title><source>MEDLINE</source><source>Free E-Journal (出版社公開部分のみ)</source><source>J-STAGE</source><creator>IIZUKA, Maki ; AYAORI, Makoto ; UTO-KONDO, Harumi ; YAKUSHIJI, Emi ; TAKIGUCHI, Shunichi ; NAKAYA, Kazuhiro ; HISADA, Tetsuya ; SASAKI, Makoto ; KOMATSU, Tomohiro ; YOGO, Makiko ; KISHIMOTO, Yoshimi ; KONDO, Kazuo ; IKEWAKI, Katsunori</creator><creatorcontrib>IIZUKA, Maki ; AYAORI, Makoto ; UTO-KONDO, Harumi ; YAKUSHIJI, Emi ; TAKIGUCHI, Shunichi ; NAKAYA, Kazuhiro ; HISADA, Tetsuya ; SASAKI, Makoto ; KOMATSU, Tomohiro ; YOGO, Makiko ; KISHIMOTO, Yoshimi ; KONDO, Kazuo ; IKEWAKI, Katsunori</creatorcontrib><description>ATP-binding cassette transporters (ABC) A1 and G1 are key molecules in cholesterol efflux from macrophages, which is an initial step of reverse cholesterol transport (RCT), a major anti-atherogenic property of high-density lipoprotein (HDL). Astaxanthin is one of the naturally occurring carotenoids responsible for the pink-red pigmentation in a variety of living organisms. Although astaxanthin is known to be a strong antioxidant, it remains unclear through what mechanism of action it affects cholesterol homeostasis in macrophages. We therefore investigated the effects of astaxanthin on cholesterol efflux and ABCA1/G1 expressions in macrophages. Astaxanthin enhanced both apolipoprotein (apo) A-I- and HDL-mediated cholesterol efflux from RAW264.7 cells. In supporting these enhanced cholesterol efflux mechanisms, astaxanthin promoted ABCA1/G1 expression in various macrophages. In contrast, peroxisome proliferator-activated receptor γ, liver X receptor (LXR) α and LXRβ levels remained unchanged by astaxanthin. An experiment using actinomycin D demonstrated that astaxanthin transcriptionally induced ABCA1/G1 expression, and oxysterol depletion caused by overexpression of cholesterol sulfotransferase further revealed that these inductions in ABCA1/G1 were independent of LXR-mediated pathways. Finally, we performed luciferase assays using human ABCA1/G1 promoter-reporter constructs to reveal that astaxanthin activated both promoters irrespective of the presence or absence of LXR-responsive elements, indicating LXR-independence of these activations. In conclusion, astaxanthin increased ABCA1/G1 expression, thereby enhancing apoA-I/HDL-mediated cholesterol efflux from the macrophages in an LXR-independent manner. In addition to the anti-oxidative properties, the potential cardioprotective properties of astaxanthin might therefore be associated with an enhanced anti-atherogenic function of HDL.</description><identifier>ISSN: 0301-4800</identifier><identifier>EISSN: 1881-7742</identifier><identifier>DOI: 10.3177/jnsv.58.96</identifier><identifier>PMID: 22790567</identifier><language>eng</language><publisher>Tokyo: Center for Academic Publications Japan</publisher><subject>ABCA1 ; ABCG1 ; Animals ; Antioxidants ; Apolipoprotein A-I - drug effects ; Apolipoprotein A-I - physiology ; astaxanthin ; ATP Binding Cassette Transporter 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 1 ; ATP-Binding Cassette Transporters - genetics ; ATP-Binding Cassette Transporters - physiology ; Biological and medical sciences ; Cardiotonic Agents ; Cell Line ; Cholesterol - metabolism ; cholesterol efflux ; Feeding. Feeding behavior ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; HDL ; Lipoproteins - genetics ; Lipoproteins - physiology ; Lipoproteins, HDL - drug effects ; Lipoproteins, HDL - physiology ; Liver X Receptors ; Macrophages - drug effects ; Macrophages - metabolism ; Mice ; Mice, Inbred C57BL ; Orphan Nuclear Receptors - physiology ; Vertebrates: anatomy and physiology, studies on body, several organs or systems ; Xanthophylls - pharmacology</subject><ispartof>Journal of Nutritional Science and Vitaminology, 2012, Vol.58(2), pp.96-104</ispartof><rights>2012 by the Center for Academic Publications Japan</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c581t-f9354216015eea8f9830ff6a751d5ddaf2210d91b02b8685578edd3e1d4212f13</citedby><cites>FETCH-LOGICAL-c581t-f9354216015eea8f9830ff6a751d5ddaf2210d91b02b8685578edd3e1d4212f13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=26020063$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22790567$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>IIZUKA, Maki</creatorcontrib><creatorcontrib>AYAORI, Makoto</creatorcontrib><creatorcontrib>UTO-KONDO, Harumi</creatorcontrib><creatorcontrib>YAKUSHIJI, Emi</creatorcontrib><creatorcontrib>TAKIGUCHI, Shunichi</creatorcontrib><creatorcontrib>NAKAYA, Kazuhiro</creatorcontrib><creatorcontrib>HISADA, Tetsuya</creatorcontrib><creatorcontrib>SASAKI, Makoto</creatorcontrib><creatorcontrib>KOMATSU, Tomohiro</creatorcontrib><creatorcontrib>YOGO, Makiko</creatorcontrib><creatorcontrib>KISHIMOTO, Yoshimi</creatorcontrib><creatorcontrib>KONDO, Kazuo</creatorcontrib><creatorcontrib>IKEWAKI, Katsunori</creatorcontrib><title>Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages</title><title>Journal of Nutritional Science and Vitaminology</title><addtitle>J Nutr Sci Vitaminol</addtitle><description>ATP-binding cassette transporters (ABC) A1 and G1 are key molecules in cholesterol efflux from macrophages, which is an initial step of reverse cholesterol transport (RCT), a major anti-atherogenic property of high-density lipoprotein (HDL). Astaxanthin is one of the naturally occurring carotenoids responsible for the pink-red pigmentation in a variety of living organisms. Although astaxanthin is known to be a strong antioxidant, it remains unclear through what mechanism of action it affects cholesterol homeostasis in macrophages. We therefore investigated the effects of astaxanthin on cholesterol efflux and ABCA1/G1 expressions in macrophages. Astaxanthin enhanced both apolipoprotein (apo) A-I- and HDL-mediated cholesterol efflux from RAW264.7 cells. In supporting these enhanced cholesterol efflux mechanisms, astaxanthin promoted ABCA1/G1 expression in various macrophages. In contrast, peroxisome proliferator-activated receptor γ, liver X receptor (LXR) α and LXRβ levels remained unchanged by astaxanthin. An experiment using actinomycin D demonstrated that astaxanthin transcriptionally induced ABCA1/G1 expression, and oxysterol depletion caused by overexpression of cholesterol sulfotransferase further revealed that these inductions in ABCA1/G1 were independent of LXR-mediated pathways. Finally, we performed luciferase assays using human ABCA1/G1 promoter-reporter constructs to reveal that astaxanthin activated both promoters irrespective of the presence or absence of LXR-responsive elements, indicating LXR-independence of these activations. In conclusion, astaxanthin increased ABCA1/G1 expression, thereby enhancing apoA-I/HDL-mediated cholesterol efflux from the macrophages in an LXR-independent manner. In addition to the anti-oxidative properties, the potential cardioprotective properties of astaxanthin might therefore be associated with an enhanced anti-atherogenic function of HDL.</description><subject>ABCA1</subject><subject>ABCG1</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apolipoprotein A-I - drug effects</subject><subject>Apolipoprotein A-I - physiology</subject><subject>astaxanthin</subject><subject>ATP Binding Cassette Transporter 1</subject><subject>ATP Binding Cassette Transporter, Subfamily G, Member 1</subject><subject>ATP-Binding Cassette Transporters - genetics</subject><subject>ATP-Binding Cassette Transporters - physiology</subject><subject>Biological and medical sciences</subject><subject>Cardiotonic Agents</subject><subject>Cell Line</subject><subject>Cholesterol - metabolism</subject><subject>cholesterol efflux</subject><subject>Feeding. Feeding behavior</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>HDL</subject><subject>Lipoproteins - genetics</subject><subject>Lipoproteins - physiology</subject><subject>Lipoproteins, HDL - drug effects</subject><subject>Lipoproteins, HDL - physiology</subject><subject>Liver X Receptors</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Orphan Nuclear Receptors - physiology</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><subject>Xanthophylls - pharmacology</subject><issn>0301-4800</issn><issn>1881-7742</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0cuO0zAUBmALgZjOwIYHQN4gIaR0fIljZ8GiU5UBaRAsyjpy4-MmVWoHn3RU3h5XLWVlyf7ORb8JecfZXHKt73cBn-fKzOvqBZlxY3ihdSlekhmTjBelYeyG3CLuGCtrU5rX5EYIXTNV6RmJC5zs0Yap6wNdhc6GFpAu1j-Lhz64Pmzp0iLCNAFdJxtwjGmCRBf8_pHT1XFMgNjHgNQGR5ddHADzexzoyvvhcKQ-xT39btsUx85uAd-QV94OCG8v5x359WW1Xn4tnn48flsunopWGT4VvpaqFLxiXAFY42sjmfeV1Yo75Zz1QnDmar5hYmMqo5Q24JwE7nKV8FzekY_nvmOKvw95qWbfYwvDYAPEAzZcasEUM-JEP51pXhIxgW_G1O9t-tNw1pwCbk4BN8o0dZXx-0vfw2YP7kr_JZrBhwuw2NrB59DaHv-7ignGKpnd57Pb5Q_YwhXYNPXtANeZ4jz4et92NjUQ5F_o4Zql</recordid><startdate>2012</startdate><enddate>2012</enddate><creator>IIZUKA, Maki</creator><creator>AYAORI, Makoto</creator><creator>UTO-KONDO, Harumi</creator><creator>YAKUSHIJI, Emi</creator><creator>TAKIGUCHI, Shunichi</creator><creator>NAKAYA, Kazuhiro</creator><creator>HISADA, Tetsuya</creator><creator>SASAKI, Makoto</creator><creator>KOMATSU, Tomohiro</creator><creator>YOGO, Makiko</creator><creator>KISHIMOTO, Yoshimi</creator><creator>KONDO, Kazuo</creator><creator>IKEWAKI, Katsunori</creator><general>Center for Academic Publications Japan</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>7TS</scope></search><sort><creationdate>2012</creationdate><title>Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages</title><author>IIZUKA, Maki ; AYAORI, Makoto ; UTO-KONDO, Harumi ; YAKUSHIJI, Emi ; TAKIGUCHI, Shunichi ; NAKAYA, Kazuhiro ; HISADA, Tetsuya ; SASAKI, Makoto ; KOMATSU, Tomohiro ; YOGO, Makiko ; KISHIMOTO, Yoshimi ; KONDO, Kazuo ; IKEWAKI, Katsunori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c581t-f9354216015eea8f9830ff6a751d5ddaf2210d91b02b8685578edd3e1d4212f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>ABCA1</topic><topic>ABCG1</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apolipoprotein A-I - drug effects</topic><topic>Apolipoprotein A-I - physiology</topic><topic>astaxanthin</topic><topic>ATP Binding Cassette Transporter 1</topic><topic>ATP Binding Cassette Transporter, Subfamily G, Member 1</topic><topic>ATP-Binding Cassette Transporters - genetics</topic><topic>ATP-Binding Cassette Transporters - physiology</topic><topic>Biological and medical sciences</topic><topic>Cardiotonic Agents</topic><topic>Cell Line</topic><topic>Cholesterol - metabolism</topic><topic>cholesterol efflux</topic><topic>Feeding. Feeding behavior</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression - drug effects</topic><topic>HDL</topic><topic>Lipoproteins - genetics</topic><topic>Lipoproteins - physiology</topic><topic>Lipoproteins, HDL - drug effects</topic><topic>Lipoproteins, HDL - physiology</topic><topic>Liver X Receptors</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Orphan Nuclear Receptors - physiology</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><topic>Xanthophylls - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>IIZUKA, Maki</creatorcontrib><creatorcontrib>AYAORI, Makoto</creatorcontrib><creatorcontrib>UTO-KONDO, Harumi</creatorcontrib><creatorcontrib>YAKUSHIJI, Emi</creatorcontrib><creatorcontrib>TAKIGUCHI, Shunichi</creatorcontrib><creatorcontrib>NAKAYA, Kazuhiro</creatorcontrib><creatorcontrib>HISADA, Tetsuya</creatorcontrib><creatorcontrib>SASAKI, Makoto</creatorcontrib><creatorcontrib>KOMATSU, Tomohiro</creatorcontrib><creatorcontrib>YOGO, Makiko</creatorcontrib><creatorcontrib>KISHIMOTO, Yoshimi</creatorcontrib><creatorcontrib>KONDO, Kazuo</creatorcontrib><creatorcontrib>IKEWAKI, Katsunori</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>Physical Education Index</collection><jtitle>Journal of Nutritional Science and Vitaminology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>IIZUKA, Maki</au><au>AYAORI, Makoto</au><au>UTO-KONDO, Harumi</au><au>YAKUSHIJI, Emi</au><au>TAKIGUCHI, Shunichi</au><au>NAKAYA, Kazuhiro</au><au>HISADA, Tetsuya</au><au>SASAKI, Makoto</au><au>KOMATSU, Tomohiro</au><au>YOGO, Makiko</au><au>KISHIMOTO, Yoshimi</au><au>KONDO, Kazuo</au><au>IKEWAKI, Katsunori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages</atitle><jtitle>Journal of Nutritional Science and Vitaminology</jtitle><addtitle>J Nutr Sci Vitaminol</addtitle><date>2012</date><risdate>2012</risdate><volume>58</volume><issue>2</issue><spage>96</spage><epage>104</epage><pages>96-104</pages><issn>0301-4800</issn><eissn>1881-7742</eissn><abstract>ATP-binding cassette transporters (ABC) A1 and G1 are key molecules in cholesterol efflux from macrophages, which is an initial step of reverse cholesterol transport (RCT), a major anti-atherogenic property of high-density lipoprotein (HDL). Astaxanthin is one of the naturally occurring carotenoids responsible for the pink-red pigmentation in a variety of living organisms. Although astaxanthin is known to be a strong antioxidant, it remains unclear through what mechanism of action it affects cholesterol homeostasis in macrophages. We therefore investigated the effects of astaxanthin on cholesterol efflux and ABCA1/G1 expressions in macrophages. Astaxanthin enhanced both apolipoprotein (apo) A-I- and HDL-mediated cholesterol efflux from RAW264.7 cells. In supporting these enhanced cholesterol efflux mechanisms, astaxanthin promoted ABCA1/G1 expression in various macrophages. In contrast, peroxisome proliferator-activated receptor γ, liver X receptor (LXR) α and LXRβ levels remained unchanged by astaxanthin. An experiment using actinomycin D demonstrated that astaxanthin transcriptionally induced ABCA1/G1 expression, and oxysterol depletion caused by overexpression of cholesterol sulfotransferase further revealed that these inductions in ABCA1/G1 were independent of LXR-mediated pathways. Finally, we performed luciferase assays using human ABCA1/G1 promoter-reporter constructs to reveal that astaxanthin activated both promoters irrespective of the presence or absence of LXR-responsive elements, indicating LXR-independence of these activations. In conclusion, astaxanthin increased ABCA1/G1 expression, thereby enhancing apoA-I/HDL-mediated cholesterol efflux from the macrophages in an LXR-independent manner. In addition to the anti-oxidative properties, the potential cardioprotective properties of astaxanthin might therefore be associated with an enhanced anti-atherogenic function of HDL.</abstract><cop>Tokyo</cop><pub>Center for Academic Publications Japan</pub><pmid>22790567</pmid><doi>10.3177/jnsv.58.96</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0301-4800
ispartof Journal of Nutritional Science and Vitaminology, 2012, Vol.58(2), pp.96-104
issn 0301-4800
1881-7742
language eng
recordid cdi_proquest_miscellaneous_1372050821
source MEDLINE; Free E-Journal (出版社公開部分のみ); J-STAGE
subjects ABCA1
ABCG1
Animals
Antioxidants
Apolipoprotein A-I - drug effects
Apolipoprotein A-I - physiology
astaxanthin
ATP Binding Cassette Transporter 1
ATP Binding Cassette Transporter, Subfamily G, Member 1
ATP-Binding Cassette Transporters - genetics
ATP-Binding Cassette Transporters - physiology
Biological and medical sciences
Cardiotonic Agents
Cell Line
Cholesterol - metabolism
cholesterol efflux
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
Gene Expression - drug effects
HDL
Lipoproteins - genetics
Lipoproteins - physiology
Lipoproteins, HDL - drug effects
Lipoproteins, HDL - physiology
Liver X Receptors
Macrophages - drug effects
Macrophages - metabolism
Mice
Mice, Inbred C57BL
Orphan Nuclear Receptors - physiology
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Xanthophylls - pharmacology
title Astaxanthin Enhances ATP-Binding Cassette Transporter A1/G1 Expressions and Cholesterol Efflux from Macrophages
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T08%3A12%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Astaxanthin%20Enhances%20ATP-Binding%20Cassette%20Transporter%20A1/G1%20Expressions%20and%20Cholesterol%20Efflux%20from%20Macrophages&rft.jtitle=Journal%20of%20Nutritional%20Science%20and%20Vitaminology&rft.au=IIZUKA,%20Maki&rft.date=2012&rft.volume=58&rft.issue=2&rft.spage=96&rft.epage=104&rft.pages=96-104&rft.issn=0301-4800&rft.eissn=1881-7742&rft_id=info:doi/10.3177/jnsv.58.96&rft_dat=%3Cproquest_cross%3E1372050821%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1372050821&rft_id=info:pmid/22790567&rfr_iscdi=true