Antagonism of betulinic acid on LPS-mediated inhibition of ABCA1 and cholesterol efflux through inhibiting nuclear factor-kappaB signaling pathway and miR-33 expression
ATP-binding cassette transporter A1 (ABCA1) is critical in exporting cholesterol from macrophages and plays a protective role in the development of atherosclerosis. The purpose of this study was to investigate the effects of betulinic acid (BA), a pentacyclic triterpenoid, on ABCA1 expression and ch...
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| Veröffentlicht in: | PloS one 2013-09, Vol.8 (9), p.e74782 |
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| creator | Zhao, Guo-Jun Tang, Shi-Lin Lv, Yun-Cheng Ouyang, Xin-Ping He, Ping-Ping Yao, Feng Chen, Wu-Jun Lu, Qian Tang, Yan-Yan Zhang, Min Fu, Yuchang Zhang, Da-Wei Yin, Kai Tang, Chao-Ke |
| description | ATP-binding cassette transporter A1 (ABCA1) is critical in exporting cholesterol from macrophages and plays a protective role in the development of atherosclerosis. The purpose of this study was to investigate the effects of betulinic acid (BA), a pentacyclic triterpenoid, on ABCA1 expression and cholesterol efflux, and to further determine the underlying mechanism. BA promoted ABCA1 expression and cholesterol efflux, decreased cellular cholesterol and cholesterol ester content in LPS-treated macrophages. Furthermore, we found that BA promoted ABCA1 expression via down-regulation of miR-33s. The inhibition of LPS-induced NF-κB activation further decreased miR-33s expression and enhanced ABCA1 expression and cholesterol efflux when compared with BA only treatment. In addition, BA suppressed IκB phosphorylation, p65 phosphorylation and nuclear translocation, and the transcription of NF-κB-dependent related gene. Moreover, BA reduced atherosclerotic lesion size, miR-33s levels and NF-κB activation, and promoted ABCA1 expression in apoE(-/-) mice. Taken together, these results reveal a novel mechanism for the BA-mediated ABCA1 expression, which may provide new insights for developing strategies for modulating vascular inflammation and atherosclerosis. |
| doi_str_mv | 10.1371/journal.pone.0074782 |
| format | Article |
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The purpose of this study was to investigate the effects of betulinic acid (BA), a pentacyclic triterpenoid, on ABCA1 expression and cholesterol efflux, and to further determine the underlying mechanism. BA promoted ABCA1 expression and cholesterol efflux, decreased cellular cholesterol and cholesterol ester content in LPS-treated macrophages. Furthermore, we found that BA promoted ABCA1 expression via down-regulation of miR-33s. The inhibition of LPS-induced NF-κB activation further decreased miR-33s expression and enhanced ABCA1 expression and cholesterol efflux when compared with BA only treatment. In addition, BA suppressed IκB phosphorylation, p65 phosphorylation and nuclear translocation, and the transcription of NF-κB-dependent related gene. Moreover, BA reduced atherosclerotic lesion size, miR-33s levels and NF-κB activation, and promoted ABCA1 expression in apoE(-/-) mice. Taken together, these results reveal a novel mechanism for the BA-mediated ABCA1 expression, which may provide new insights for developing strategies for modulating vascular inflammation and atherosclerosis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0074782</identifier><identifier>PMID: 24086374</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>ABCA1 protein ; Acids ; Activation ; Animals ; Apolipoprotein E ; Apolipoproteins ; Apolipoproteins E - deficiency ; Apolipoproteins E - metabolism ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - blood ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; ATP Binding Cassette Transporter 1 - antagonists & inhibitors ; ATP Binding Cassette Transporter 1 - metabolism ; ATP-binding protein ; Betulinic acid ; Biological Transport - drug effects ; Body Weight - drug effects ; Cell Line ; Cell Nucleus - drug effects ; Cell Nucleus - metabolism ; Cholesterol ; Cholesterol - metabolism ; Cytokines ; Development and progression ; Efflux ; Gene Expression Regulation - drug effects ; Genetic transcription ; Humans ; Inflammation ; Inhibition ; Kinases ; Laboratories ; Lipids ; Lipids - blood ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Metabolism ; Mice ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Models, Biological ; NF-kappa B - metabolism ; NF-κB protein ; Nuclear transport ; Phosphorylation ; Protein Transport - drug effects ; Rodents ; Signal transduction ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Signaling ; Transcription ; Translocation ; Transporter ; Triterpenes - antagonists & inhibitors ; Triterpenes - pharmacology</subject><ispartof>PloS one, 2013-09, Vol.8 (9), p.e74782</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Zhao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (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>2013 Zhao et al 2013 Zhao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-42c0f0b72559e0bbb6d742af22d758308e09cb2774303a58dc023e56f5c0ffa13</citedby><cites>FETCH-LOGICAL-c692t-42c0f0b72559e0bbb6d742af22d758308e09cb2774303a58dc023e56f5c0ffa13</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/PMC3783495/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783495/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24086374$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Valledor, Annabel</contributor><creatorcontrib>Zhao, Guo-Jun</creatorcontrib><creatorcontrib>Tang, Shi-Lin</creatorcontrib><creatorcontrib>Lv, Yun-Cheng</creatorcontrib><creatorcontrib>Ouyang, Xin-Ping</creatorcontrib><creatorcontrib>He, Ping-Ping</creatorcontrib><creatorcontrib>Yao, Feng</creatorcontrib><creatorcontrib>Chen, Wu-Jun</creatorcontrib><creatorcontrib>Lu, Qian</creatorcontrib><creatorcontrib>Tang, Yan-Yan</creatorcontrib><creatorcontrib>Zhang, Min</creatorcontrib><creatorcontrib>Fu, Yuchang</creatorcontrib><creatorcontrib>Zhang, Da-Wei</creatorcontrib><creatorcontrib>Yin, Kai</creatorcontrib><creatorcontrib>Tang, Chao-Ke</creatorcontrib><title>Antagonism of betulinic acid on LPS-mediated inhibition of ABCA1 and cholesterol efflux through inhibiting nuclear factor-kappaB signaling pathway and miR-33 expression</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>ATP-binding cassette transporter A1 (ABCA1) is critical in exporting cholesterol from macrophages and plays a protective role in the development of atherosclerosis. The purpose of this study was to investigate the effects of betulinic acid (BA), a pentacyclic triterpenoid, on ABCA1 expression and cholesterol efflux, and to further determine the underlying mechanism. BA promoted ABCA1 expression and cholesterol efflux, decreased cellular cholesterol and cholesterol ester content in LPS-treated macrophages. Furthermore, we found that BA promoted ABCA1 expression via down-regulation of miR-33s. The inhibition of LPS-induced NF-κB activation further decreased miR-33s expression and enhanced ABCA1 expression and cholesterol efflux when compared with BA only treatment. In addition, BA suppressed IκB phosphorylation, p65 phosphorylation and nuclear translocation, and the transcription of NF-κB-dependent related gene. Moreover, BA reduced atherosclerotic lesion size, miR-33s levels and NF-κB activation, and promoted ABCA1 expression in apoE(-/-) mice. Taken together, these results reveal a novel mechanism for the BA-mediated ABCA1 expression, which may provide new insights for developing strategies for modulating vascular inflammation and atherosclerosis.</description><subject>ABCA1 protein</subject><subject>Acids</subject><subject>Activation</subject><subject>Animals</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - metabolism</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>ATP Binding Cassette Transporter 1 - antagonists & inhibitors</subject><subject>ATP Binding Cassette Transporter 1 - metabolism</subject><subject>ATP-binding protein</subject><subject>Betulinic acid</subject><subject>Biological Transport - drug effects</subject><subject>Body Weight - drug effects</subject><subject>Cell Line</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - metabolism</subject><subject>Cholesterol</subject><subject>Cholesterol - metabolism</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Efflux</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genetic transcription</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inhibition</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lipids</subject><subject>Lipids - blood</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mice</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Models, Biological</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Phosphorylation</subject><subject>Protein Transport - drug effects</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Signaling</subject><subject>Transcription</subject><subject>Translocation</subject><subject>Transporter</subject><subject>Triterpenes - antagonists & inhibitors</subject><subject>Triterpenes - pharmacology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk12L1DAUhoso7jr6D0QDguBFxzQfTXsjzA5-DCys7Kq3IU2TNmsnqUmqu__In2lmp7vsgIL0IuXked-TnJyTZc8LuCwwK95euslbMSxHZ9USQkZYhR5kx0WNUV4iiB_e-z_KnoRwCSHFVVk-zo4QgVWJGTnOfq9sFJ2zJmyB06BRcRqMNRIIaVrgLDj9fJFvVWtEVC0wtjeNiSbFE7w6Wa8KIGwLZO8GFaLybgBK62G6ArH3bur6O4ntgJ3koIQHWsjofP5djKM4AcF06Rq7_VHE_pe4vnHcmvMcY6CuRq9CSAmfZo-0GIJ6Nq-L7OuH91_Wn_LTs4-b9eo0l2WNYk6QhBo2DFFaK9g0TdkygoRGqGW0wrBSsJYNYoxgiAWtWgkRVrTUNOm0KPAie7n3HQcX-FzkwAuCS1aRgpJEbPZE68QlH73ZCn_NnTD8JuB8x4WPJt2Vl5RVWKZkkDakkoXQmilal1S1hS4JSl7v5mxTk6oslY1eDAemhzvW9LxzPzlOxqSmyeDVbODdjym9wT-OPFOdSKcyVrtkJrcmSL4ijNU1palXFtnyL1T6WrU1MrWZNil-IHhzIEhMVFexE1MIfHNx_v_s2bdD9vU9tldiiH1ww7RrvHAIkj0ovQvBK31XuQLy3ZTcVoPvpoTPU5JkL-5X_U50Oxb4D6NjDvs</recordid><startdate>20130925</startdate><enddate>20130925</enddate><creator>Zhao, Guo-Jun</creator><creator>Tang, Shi-Lin</creator><creator>Lv, Yun-Cheng</creator><creator>Ouyang, Xin-Ping</creator><creator>He, Ping-Ping</creator><creator>Yao, Feng</creator><creator>Chen, Wu-Jun</creator><creator>Lu, Qian</creator><creator>Tang, Yan-Yan</creator><creator>Zhang, Min</creator><creator>Fu, Yuchang</creator><creator>Zhang, Da-Wei</creator><creator>Yin, Kai</creator><creator>Tang, Chao-Ke</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>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>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130925</creationdate><title>Antagonism of betulinic acid on LPS-mediated inhibition of ABCA1 and cholesterol efflux through inhibiting nuclear factor-kappaB signaling pathway and miR-33 expression</title><author>Zhao, Guo-Jun ; Tang, Shi-Lin ; Lv, Yun-Cheng ; Ouyang, Xin-Ping ; He, Ping-Ping ; Yao, Feng ; Chen, Wu-Jun ; Lu, Qian ; Tang, Yan-Yan ; Zhang, Min ; Fu, Yuchang ; Zhang, Da-Wei ; Yin, Kai ; Tang, Chao-Ke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-42c0f0b72559e0bbb6d742af22d758308e09cb2774303a58dc023e56f5c0ffa13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>ABCA1 protein</topic><topic>Acids</topic><topic>Activation</topic><topic>Animals</topic><topic>Apolipoprotein E</topic><topic>Apolipoproteins</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - metabolism</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - blood</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>ATP Binding Cassette Transporter 1 - antagonists & inhibitors</topic><topic>ATP Binding Cassette Transporter 1 - metabolism</topic><topic>ATP-binding protein</topic><topic>Betulinic acid</topic><topic>Biological Transport - drug effects</topic><topic>Body Weight - drug effects</topic><topic>Cell Line</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - metabolism</topic><topic>Cholesterol</topic><topic>Cholesterol - metabolism</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Efflux</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genetic transcription</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inhibition</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Lipids</topic><topic>Lipids - 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The purpose of this study was to investigate the effects of betulinic acid (BA), a pentacyclic triterpenoid, on ABCA1 expression and cholesterol efflux, and to further determine the underlying mechanism. BA promoted ABCA1 expression and cholesterol efflux, decreased cellular cholesterol and cholesterol ester content in LPS-treated macrophages. Furthermore, we found that BA promoted ABCA1 expression via down-regulation of miR-33s. The inhibition of LPS-induced NF-κB activation further decreased miR-33s expression and enhanced ABCA1 expression and cholesterol efflux when compared with BA only treatment. In addition, BA suppressed IκB phosphorylation, p65 phosphorylation and nuclear translocation, and the transcription of NF-κB-dependent related gene. Moreover, BA reduced atherosclerotic lesion size, miR-33s levels and NF-κB activation, and promoted ABCA1 expression in apoE(-/-) mice. Taken together, these results reveal a novel mechanism for the BA-mediated ABCA1 expression, which may provide new insights for developing strategies for modulating vascular inflammation and atherosclerosis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24086374</pmid><doi>10.1371/journal.pone.0074782</doi><tpages>e74782</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-09, Vol.8 (9), p.e74782 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1436784154 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | ABCA1 protein Acids Activation Animals Apolipoprotein E Apolipoproteins Apolipoproteins E - deficiency Apolipoproteins E - metabolism Arteriosclerosis Atherosclerosis Atherosclerosis - blood Atherosclerosis - metabolism Atherosclerosis - pathology ATP Binding Cassette Transporter 1 - antagonists & inhibitors ATP Binding Cassette Transporter 1 - metabolism ATP-binding protein Betulinic acid Biological Transport - drug effects Body Weight - drug effects Cell Line Cell Nucleus - drug effects Cell Nucleus - metabolism Cholesterol Cholesterol - metabolism Cytokines Development and progression Efflux Gene Expression Regulation - drug effects Genetic transcription Humans Inflammation Inhibition Kinases Laboratories Lipids Lipids - blood Lipopolysaccharides Lipopolysaccharides - pharmacology Macrophages Macrophages - drug effects Macrophages - metabolism Male Metabolism Mice MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Models, Biological NF-kappa B - metabolism NF-κB protein Nuclear transport Phosphorylation Protein Transport - drug effects Rodents Signal transduction Signal Transduction - drug effects Signal Transduction - genetics Signaling Transcription Translocation Transporter Triterpenes - antagonists & inhibitors Triterpenes - pharmacology |
| title | Antagonism of betulinic acid on LPS-mediated inhibition of ABCA1 and cholesterol efflux through inhibiting nuclear factor-kappaB signaling pathway and miR-33 expression |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T20%3A39%3A19IST&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=Antagonism%20of%20betulinic%20acid%20on%20LPS-mediated%20inhibition%20of%20ABCA1%20and%20cholesterol%20efflux%20through%20inhibiting%20nuclear%20factor-kappaB%20signaling%20pathway%20and%20miR-33%20expression&rft.jtitle=PloS%20one&rft.au=Zhao,%20Guo-Jun&rft.date=2013-09-25&rft.volume=8&rft.issue=9&rft.spage=e74782&rft.pages=e74782-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0074782&rft_dat=%3Cgale_plos_%3EA477995519%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=1436784154&rft_id=info:pmid/24086374&rft_galeid=A477995519&rft_doaj_id=oai_doaj_org_article_65783c77405b48c1aff7e5965ed1f642&rfr_iscdi=true |