HDL activates expression of genes stimulating cholesterol efflux in human monocyte-derived macrophages
High density lipoproteins (HDL) are key components of reverse cholesterol transport pathway. HDL removes excessive cholesterol from peripheral cells, including macrophages, providing protection from cholesterol accumulation and conversion into foam cells, which is a key event in pathogenesis of athe...
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| Veröffentlicht in: | Experimental and molecular pathology 2018-10, Vol.105 (2), p.202-207 |
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| creator | Orekhov, Alexander N. Pushkarsky, Tatiana Oishi, Yumiko Nikiforov, Nikita G. Zhelankin, Andrey V. Dubrovsky, Larisa Makeev, Vsevolod J. Foxx, Kathy Jin, Xueting Kruth, Howard S. Sobenin, Igor A. Sukhorukov, Vasily N. Zakiev, Emile R. Kontush, Anatol Le Goff, Wilfried Bukrinsky, Michael |
| description | High density lipoproteins (HDL) are key components of reverse cholesterol transport pathway. HDL removes excessive cholesterol from peripheral cells, including macrophages, providing protection from cholesterol accumulation and conversion into foam cells, which is a key event in pathogenesis of atherosclerosis. The mechanism of cellular cholesterol efflux stimulation by HDL involves interaction with the ABCA1 lipid transporter and ensuing transfer of cholesterol to HDL particles. In this study, we looked for additional proteins contributing to HDL-dependent cholesterol efflux. Using RNAseq, we analyzed mRNAs induced by HDL in human monocyte-derived macrophages and identified three genes, fatty acid desaturase 1 (FADS1), insulin induced gene 1 (INSIG1), and the low-density lipoprotein receptor (LDLR), expression of which was significantly upregulated by HDL. We individually knocked down these genes in THP-1 cells using gene silencing by siRNA, and measured cellular cholesterol efflux to HDL. Knock down of FADS1 did not significantly change cholesterol efflux (p = 0.70), but knockdown of INSIG1 and LDLR resulted in highly significant reduction of the efflux to HDL (67% and 75% of control, respectively, p |
| doi_str_mv | 10.1016/j.yexmp.2018.08.003 |
| format | Article |
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HDL removes excessive cholesterol from peripheral cells, including macrophages, providing protection from cholesterol accumulation and conversion into foam cells, which is a key event in pathogenesis of atherosclerosis. The mechanism of cellular cholesterol efflux stimulation by HDL involves interaction with the ABCA1 lipid transporter and ensuing transfer of cholesterol to HDL particles. In this study, we looked for additional proteins contributing to HDL-dependent cholesterol efflux. Using RNAseq, we analyzed mRNAs induced by HDL in human monocyte-derived macrophages and identified three genes, fatty acid desaturase 1 (FADS1), insulin induced gene 1 (INSIG1), and the low-density lipoprotein receptor (LDLR), expression of which was significantly upregulated by HDL. We individually knocked down these genes in THP-1 cells using gene silencing by siRNA, and measured cellular cholesterol efflux to HDL. Knock down of FADS1 did not significantly change cholesterol efflux (p = 0.70), but knockdown of INSIG1 and LDLR resulted in highly significant reduction of the efflux to HDL (67% and 75% of control, respectively, p < 0.001). Importantly, the suppression of cholesterol efflux was independent of known effects of these genes on cellular cholesterol content, as cells were loaded with cholesterol using acetylated LDL. These results indicate that HDL particles stimulate expression of genes that enhance cellular cholesterol transfer to HDL.</description><identifier>ISSN: 0014-4800</identifier><identifier>EISSN: 1096-0945</identifier><identifier>DOI: 10.1016/j.yexmp.2018.08.003</identifier><identifier>PMID: 30118702</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Atherosclerosis ; Atherosclerosis - physiopathology ; ATP Binding Cassette Transporter 1 - genetics ; Biological Transport ; Cholesterol ; Cholesterol efflux ; Cholesterol, HDL - genetics ; Cholesterol, HDL - metabolism ; Fatty Acid Desaturases - genetics ; Fatty Acid Desaturases - metabolism ; Foam Cells ; Gene Expression Profiling ; Gene Expression Regulation - genetics ; Gene Silencing ; HDL ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Life Sciences ; Lipid metabolism ; Lipoproteins, HDL - genetics ; Lipoproteins, HDL - metabolism ; Macrophages - metabolism ; Macrophages - physiology ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Monocyte-derived macrophages ; Receptors, LDL - genetics ; Receptors, LDL - metabolism ; RNA, Messenger ; RNA, Small Interfering ; THP-1 Cells ; Transcriptome analysis ; Up-Regulation</subject><ispartof>Experimental and molecular pathology, 2018-10, Vol.105 (2), p.202-207</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c493t-8bece0122931f417e8b873ad6f4188a914e856f569ca0c1956fcb5faac4261283</citedby><cites>FETCH-LOGICAL-c493t-8bece0122931f417e8b873ad6f4188a914e856f569ca0c1956fcb5faac4261283</cites><orcidid>0000-0002-8593-0770</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.yexmp.2018.08.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30118702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03625006$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Orekhov, Alexander N.</creatorcontrib><creatorcontrib>Pushkarsky, Tatiana</creatorcontrib><creatorcontrib>Oishi, Yumiko</creatorcontrib><creatorcontrib>Nikiforov, Nikita G.</creatorcontrib><creatorcontrib>Zhelankin, Andrey V.</creatorcontrib><creatorcontrib>Dubrovsky, Larisa</creatorcontrib><creatorcontrib>Makeev, Vsevolod J.</creatorcontrib><creatorcontrib>Foxx, Kathy</creatorcontrib><creatorcontrib>Jin, Xueting</creatorcontrib><creatorcontrib>Kruth, Howard S.</creatorcontrib><creatorcontrib>Sobenin, Igor A.</creatorcontrib><creatorcontrib>Sukhorukov, Vasily N.</creatorcontrib><creatorcontrib>Zakiev, Emile R.</creatorcontrib><creatorcontrib>Kontush, Anatol</creatorcontrib><creatorcontrib>Le Goff, Wilfried</creatorcontrib><creatorcontrib>Bukrinsky, Michael</creatorcontrib><title>HDL activates expression of genes stimulating cholesterol efflux in human monocyte-derived macrophages</title><title>Experimental and molecular pathology</title><addtitle>Exp Mol Pathol</addtitle><description>High density lipoproteins (HDL) are key components of reverse cholesterol transport pathway. HDL removes excessive cholesterol from peripheral cells, including macrophages, providing protection from cholesterol accumulation and conversion into foam cells, which is a key event in pathogenesis of atherosclerosis. The mechanism of cellular cholesterol efflux stimulation by HDL involves interaction with the ABCA1 lipid transporter and ensuing transfer of cholesterol to HDL particles. In this study, we looked for additional proteins contributing to HDL-dependent cholesterol efflux. Using RNAseq, we analyzed mRNAs induced by HDL in human monocyte-derived macrophages and identified three genes, fatty acid desaturase 1 (FADS1), insulin induced gene 1 (INSIG1), and the low-density lipoprotein receptor (LDLR), expression of which was significantly upregulated by HDL. We individually knocked down these genes in THP-1 cells using gene silencing by siRNA, and measured cellular cholesterol efflux to HDL. Knock down of FADS1 did not significantly change cholesterol efflux (p = 0.70), but knockdown of INSIG1 and LDLR resulted in highly significant reduction of the efflux to HDL (67% and 75% of control, respectively, p < 0.001). Importantly, the suppression of cholesterol efflux was independent of known effects of these genes on cellular cholesterol content, as cells were loaded with cholesterol using acetylated LDL. These results indicate that HDL particles stimulate expression of genes that enhance cellular cholesterol transfer to HDL.</description><subject>Atherosclerosis</subject><subject>Atherosclerosis - physiopathology</subject><subject>ATP Binding Cassette Transporter 1 - genetics</subject><subject>Biological Transport</subject><subject>Cholesterol</subject><subject>Cholesterol efflux</subject><subject>Cholesterol, HDL - genetics</subject><subject>Cholesterol, HDL - metabolism</subject><subject>Fatty Acid Desaturases - genetics</subject><subject>Fatty Acid Desaturases - metabolism</subject><subject>Foam Cells</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene Silencing</subject><subject>HDL</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Life Sciences</subject><subject>Lipid metabolism</subject><subject>Lipoproteins, HDL - genetics</subject><subject>Lipoproteins, HDL - metabolism</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - physiology</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Monocyte-derived macrophages</subject><subject>Receptors, LDL - genetics</subject><subject>Receptors, LDL - metabolism</subject><subject>RNA, Messenger</subject><subject>RNA, Small Interfering</subject><subject>THP-1 Cells</subject><subject>Transcriptome analysis</subject><subject>Up-Regulation</subject><issn>0014-4800</issn><issn>1096-0945</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU2P0zAUtBCI7S78AiTkIxxSnu18OAeQVgtLkSpxgbPlOi-Nq8QOdhK1_x6XLivggPQk288z8-wZQl4xWDNg5bvD-oTHYVxzYHINqUA8ISsGdZlBnRdPyQqA5VkuAa7IdYwHAKiB8efkSgBjsgK-Iu3m45ZqM9lFTxgpHseAMVrvqG_pHl3qxckOc68n6_bUdL7HOGHwPcW27ecjtY5286AdHbzz5jRh1mCwCzZ00Cb4sdN7jC_Is1b3EV8-rDfk-_2nb3ebbPv185e7221m8lpMmdyhwfREXgvW5qxCuZOV0E2ZDlLqmuUoi7ItytpoMKxOe7MrWq1NzkvGpbghHy6647wbsDHopqB7NQY76HBSXlv1942zndr7RZU8rySwJPD2ItD9Q9vcbtW5B6LkBUC5nLFvHoYF_2NOtqjBRoN9rx36OSoOspZFVQieoOICTY7EGLB91Gagzmmqg_qVpjqnqSAViMR6_edvHjm_40uA9xcAJk8Xi0FFY9EZbGxAM6nG2_8O-AlZerQU</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Orekhov, Alexander N.</creator><creator>Pushkarsky, Tatiana</creator><creator>Oishi, Yumiko</creator><creator>Nikiforov, Nikita G.</creator><creator>Zhelankin, Andrey V.</creator><creator>Dubrovsky, Larisa</creator><creator>Makeev, Vsevolod J.</creator><creator>Foxx, Kathy</creator><creator>Jin, Xueting</creator><creator>Kruth, Howard S.</creator><creator>Sobenin, Igor A.</creator><creator>Sukhorukov, Vasily N.</creator><creator>Zakiev, Emile R.</creator><creator>Kontush, Anatol</creator><creator>Le Goff, Wilfried</creator><creator>Bukrinsky, Michael</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope><scope>1XC</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8593-0770</orcidid></search><sort><creationdate>20181001</creationdate><title>HDL activates expression of genes stimulating cholesterol efflux in human monocyte-derived macrophages</title><author>Orekhov, Alexander N. ; Pushkarsky, Tatiana ; Oishi, Yumiko ; Nikiforov, Nikita G. ; Zhelankin, Andrey V. ; Dubrovsky, Larisa ; Makeev, Vsevolod J. ; Foxx, Kathy ; Jin, Xueting ; Kruth, Howard S. ; Sobenin, Igor A. ; Sukhorukov, Vasily N. ; Zakiev, Emile R. ; Kontush, Anatol ; Le Goff, Wilfried ; Bukrinsky, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c493t-8bece0122931f417e8b873ad6f4188a914e856f569ca0c1956fcb5faac4261283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Atherosclerosis</topic><topic>Atherosclerosis - physiopathology</topic><topic>ATP Binding Cassette Transporter 1 - genetics</topic><topic>Biological Transport</topic><topic>Cholesterol</topic><topic>Cholesterol efflux</topic><topic>Cholesterol, HDL - genetics</topic><topic>Cholesterol, HDL - metabolism</topic><topic>Fatty Acid Desaturases - genetics</topic><topic>Fatty Acid Desaturases - metabolism</topic><topic>Foam Cells</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - genetics</topic><topic>Gene Silencing</topic><topic>HDL</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Life Sciences</topic><topic>Lipid metabolism</topic><topic>Lipoproteins, HDL - genetics</topic><topic>Lipoproteins, HDL - metabolism</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - physiology</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Monocyte-derived macrophages</topic><topic>Receptors, LDL - genetics</topic><topic>Receptors, LDL - metabolism</topic><topic>RNA, Messenger</topic><topic>RNA, Small Interfering</topic><topic>THP-1 Cells</topic><topic>Transcriptome analysis</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Orekhov, Alexander N.</creatorcontrib><creatorcontrib>Pushkarsky, Tatiana</creatorcontrib><creatorcontrib>Oishi, Yumiko</creatorcontrib><creatorcontrib>Nikiforov, Nikita G.</creatorcontrib><creatorcontrib>Zhelankin, Andrey V.</creatorcontrib><creatorcontrib>Dubrovsky, Larisa</creatorcontrib><creatorcontrib>Makeev, Vsevolod J.</creatorcontrib><creatorcontrib>Foxx, Kathy</creatorcontrib><creatorcontrib>Jin, Xueting</creatorcontrib><creatorcontrib>Kruth, Howard S.</creatorcontrib><creatorcontrib>Sobenin, Igor A.</creatorcontrib><creatorcontrib>Sukhorukov, Vasily N.</creatorcontrib><creatorcontrib>Zakiev, Emile R.</creatorcontrib><creatorcontrib>Kontush, Anatol</creatorcontrib><creatorcontrib>Le Goff, Wilfried</creatorcontrib><creatorcontrib>Bukrinsky, Michael</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and molecular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Orekhov, Alexander N.</au><au>Pushkarsky, Tatiana</au><au>Oishi, Yumiko</au><au>Nikiforov, Nikita G.</au><au>Zhelankin, Andrey V.</au><au>Dubrovsky, Larisa</au><au>Makeev, Vsevolod J.</au><au>Foxx, Kathy</au><au>Jin, Xueting</au><au>Kruth, Howard S.</au><au>Sobenin, Igor A.</au><au>Sukhorukov, Vasily N.</au><au>Zakiev, Emile R.</au><au>Kontush, Anatol</au><au>Le Goff, Wilfried</au><au>Bukrinsky, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HDL activates expression of genes stimulating cholesterol efflux in human monocyte-derived macrophages</atitle><jtitle>Experimental and molecular pathology</jtitle><addtitle>Exp Mol Pathol</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>105</volume><issue>2</issue><spage>202</spage><epage>207</epage><pages>202-207</pages><issn>0014-4800</issn><eissn>1096-0945</eissn><abstract>High density lipoproteins (HDL) are key components of reverse cholesterol transport pathway. HDL removes excessive cholesterol from peripheral cells, including macrophages, providing protection from cholesterol accumulation and conversion into foam cells, which is a key event in pathogenesis of atherosclerosis. The mechanism of cellular cholesterol efflux stimulation by HDL involves interaction with the ABCA1 lipid transporter and ensuing transfer of cholesterol to HDL particles. In this study, we looked for additional proteins contributing to HDL-dependent cholesterol efflux. Using RNAseq, we analyzed mRNAs induced by HDL in human monocyte-derived macrophages and identified three genes, fatty acid desaturase 1 (FADS1), insulin induced gene 1 (INSIG1), and the low-density lipoprotein receptor (LDLR), expression of which was significantly upregulated by HDL. We individually knocked down these genes in THP-1 cells using gene silencing by siRNA, and measured cellular cholesterol efflux to HDL. Knock down of FADS1 did not significantly change cholesterol efflux (p = 0.70), but knockdown of INSIG1 and LDLR resulted in highly significant reduction of the efflux to HDL (67% and 75% of control, respectively, p < 0.001). Importantly, the suppression of cholesterol efflux was independent of known effects of these genes on cellular cholesterol content, as cells were loaded with cholesterol using acetylated LDL. These results indicate that HDL particles stimulate expression of genes that enhance cellular cholesterol transfer to HDL.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>30118702</pmid><doi>10.1016/j.yexmp.2018.08.003</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-8593-0770</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Atherosclerosis Atherosclerosis - physiopathology ATP Binding Cassette Transporter 1 - genetics Biological Transport Cholesterol Cholesterol efflux Cholesterol, HDL - genetics Cholesterol, HDL - metabolism Fatty Acid Desaturases - genetics Fatty Acid Desaturases - metabolism Foam Cells Gene Expression Profiling Gene Expression Regulation - genetics Gene Silencing HDL Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Life Sciences Lipid metabolism Lipoproteins, HDL - genetics Lipoproteins, HDL - metabolism Macrophages - metabolism Macrophages - physiology Membrane Proteins - genetics Membrane Proteins - metabolism Monocyte-derived macrophages Receptors, LDL - genetics Receptors, LDL - metabolism RNA, Messenger RNA, Small Interfering THP-1 Cells Transcriptome analysis Up-Regulation |
| title | HDL activates expression of genes stimulating cholesterol efflux in human monocyte-derived macrophages |
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