Modulation of microRNA Expression in Subjects with Metabolic Syndrome and Decrease of Cholesterol Efflux from Macrophages via microRNA-33-Mediated Attenuation of ATP-Binding Cassette Transporter A1 Expression by Statins
Metabolic syndrome (MetS) is a complicated health problem that encompasses a variety of metabolic disorders. In this study, we analyzed the relationship between the major biochemical parameters associated with MetS and circulating levels of microRNA (miR)-33, miR-103, and miR-155. We found that miRN...
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| description | Metabolic syndrome (MetS) is a complicated health problem that encompasses a variety of metabolic disorders. In this study, we analyzed the relationship between the major biochemical parameters associated with MetS and circulating levels of microRNA (miR)-33, miR-103, and miR-155. We found that miRNA-33 levels were positively correlated with levels of fasting blood glucose, glycosylated hemoglobin A1c, total cholesterol, LDL-cholesterol, and triacylglycerol, but negatively correlated with HDL-cholesterol levels. In the cellular study, miR-33 levels were increased in macrophages treated with high glucose and cholesterol-lowering drugs atorvastatin and pitavastatin. miR-33 has been reported to play an essential role in cholesterol homeostasis through ATP-binding cassette transporter A1 (ABCA1) regulation and reverse cholesterol transport. However, the molecular mechanism underlying the linkage between miR-33 and statin treatment remains unclear. In the present study, we investigated whether atorvastatin and pitavastatin exert their functions through the modulation of miR-33 and ABCA1-mediated cholesterol efflux from macrophages. The results showed that treatment of the statins up-regulated miR-33 expression, but down-regulated ABCA1 mRNA levels in RAW264.7 cells and bone marrow-derived macrophages. Statin-mediated ABCA1 regulation occurs at the post-transcriptional level through targeting of the 3'-UTR of the ABCA1 transcript by miR-33. Additionally, we found significant down-regulation of ABCA1 protein expression in macrophages treated with statins. Finally, we showed that high glucose and statin treatment significantly suppressed cholesterol efflux from macrophages. These findings have highlighted the complexity of statins, which may exert detrimental effects on metabolic abnormalities through regulation of miR-33 target genes. |
| doi_str_mv | 10.1371/journal.pone.0154672 |
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In this study, we analyzed the relationship between the major biochemical parameters associated with MetS and circulating levels of microRNA (miR)-33, miR-103, and miR-155. We found that miRNA-33 levels were positively correlated with levels of fasting blood glucose, glycosylated hemoglobin A1c, total cholesterol, LDL-cholesterol, and triacylglycerol, but negatively correlated with HDL-cholesterol levels. In the cellular study, miR-33 levels were increased in macrophages treated with high glucose and cholesterol-lowering drugs atorvastatin and pitavastatin. miR-33 has been reported to play an essential role in cholesterol homeostasis through ATP-binding cassette transporter A1 (ABCA1) regulation and reverse cholesterol transport. However, the molecular mechanism underlying the linkage between miR-33 and statin treatment remains unclear. In the present study, we investigated whether atorvastatin and pitavastatin exert their functions through the modulation of miR-33 and ABCA1-mediated cholesterol efflux from macrophages. The results showed that treatment of the statins up-regulated miR-33 expression, but down-regulated ABCA1 mRNA levels in RAW264.7 cells and bone marrow-derived macrophages. Statin-mediated ABCA1 regulation occurs at the post-transcriptional level through targeting of the 3'-UTR of the ABCA1 transcript by miR-33. Additionally, we found significant down-regulation of ABCA1 protein expression in macrophages treated with statins. Finally, we showed that high glucose and statin treatment significantly suppressed cholesterol efflux from macrophages. These findings have highlighted the complexity of statins, which may exert detrimental effects on metabolic abnormalities through regulation of miR-33 target genes.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0154672</identifier><identifier>PMID: 27139226</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated regions ; ABC transporters ; ABCA1 protein ; Abnormalities ; Analysis ; Animals ; Atherosclerosis ; Atorvastatin ; ATP ; ATP Binding Cassette Transporter 1 - genetics ; ATP-binding protein ; Biochemistry ; Biological Transport - drug effects ; Biology and Life Sciences ; Bone marrow ; Cardiovascular disease ; Cholesterol ; Cholesterol - metabolism ; Complications and side effects ; Development and progression ; Diabetes ; Dosage and administration ; Down-Regulation - drug effects ; Down-Regulation - genetics ; Drugs ; Efflux ; Endocrinology ; Federal regulation ; Female ; Gastroenterology ; Gene expression ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - genetics ; Gene regulation ; Genetic aspects ; Glucose ; Glucose - pharmacology ; Hemoglobin ; Hepatology ; High density lipoprotein ; Homeostasis ; Homeostasis - drug effects ; Hospitals ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; Hyperglycemia ; Internal medicine ; Low density lipoprotein ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Medicine ; Medicine and Health Sciences ; Metabolic disorders ; Metabolic syndrome ; Metabolic Syndrome - genetics ; Metabolic Syndrome - metabolism ; Metabolic syndrome X ; Mice ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Middle Aged ; miRNA ; Modulation ; Molecular biology ; Physical Sciences ; Physiological aspects ; Post-transcription ; Proteins ; RAW 264.7 Cells ; Ribonucleic acid ; RNA ; Statins ; Systemic diseases</subject><ispartof>PloS one, 2016-05, Vol.11 (5), p.e0154672-e0154672</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://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>2016 Chen et al 2016 Chen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-cbd7f581f9600f7dd3385b286045e267310070dd3ff200158828a64847f54c803</citedby><cites>FETCH-LOGICAL-c725t-cbd7f581f9600f7dd3385b286045e267310070dd3ff200158828a64847f54c803</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/PMC4854384/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854384/$$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/27139226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Amodio, Nicola</contributor><creatorcontrib>Chen, Wei-Ming</creatorcontrib><creatorcontrib>Sheu, Wayne H-H</creatorcontrib><creatorcontrib>Tseng, Pei-Chi</creatorcontrib><creatorcontrib>Lee, Tzong-Shyuan</creatorcontrib><creatorcontrib>Lee, Wen-Jane</creatorcontrib><creatorcontrib>Chang, Pey-Jium</creatorcontrib><creatorcontrib>Chiang, An-Na</creatorcontrib><title>Modulation of microRNA Expression in Subjects with Metabolic Syndrome and Decrease of Cholesterol Efflux from Macrophages via microRNA-33-Mediated Attenuation of ATP-Binding Cassette Transporter A1 Expression by Statins</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Metabolic syndrome (MetS) is a complicated health problem that encompasses a variety of metabolic disorders. In this study, we analyzed the relationship between the major biochemical parameters associated with MetS and circulating levels of microRNA (miR)-33, miR-103, and miR-155. We found that miRNA-33 levels were positively correlated with levels of fasting blood glucose, glycosylated hemoglobin A1c, total cholesterol, LDL-cholesterol, and triacylglycerol, but negatively correlated with HDL-cholesterol levels. In the cellular study, miR-33 levels were increased in macrophages treated with high glucose and cholesterol-lowering drugs atorvastatin and pitavastatin. miR-33 has been reported to play an essential role in cholesterol homeostasis through ATP-binding cassette transporter A1 (ABCA1) regulation and reverse cholesterol transport. However, the molecular mechanism underlying the linkage between miR-33 and statin treatment remains unclear. In the present study, we investigated whether atorvastatin and pitavastatin exert their functions through the modulation of miR-33 and ABCA1-mediated cholesterol efflux from macrophages. The results showed that treatment of the statins up-regulated miR-33 expression, but down-regulated ABCA1 mRNA levels in RAW264.7 cells and bone marrow-derived macrophages. Statin-mediated ABCA1 regulation occurs at the post-transcriptional level through targeting of the 3'-UTR of the ABCA1 transcript by miR-33. Additionally, we found significant down-regulation of ABCA1 protein expression in macrophages treated with statins. Finally, we showed that high glucose and statin treatment significantly suppressed cholesterol efflux from macrophages. These findings have highlighted the complexity of statins, which may exert detrimental effects on metabolic abnormalities through regulation of miR-33 target genes.</description><subject>3' Untranslated regions</subject><subject>ABC transporters</subject><subject>ABCA1 protein</subject><subject>Abnormalities</subject><subject>Analysis</subject><subject>Animals</subject><subject>Atherosclerosis</subject><subject>Atorvastatin</subject><subject>ATP</subject><subject>ATP Binding Cassette Transporter 1 - genetics</subject><subject>ATP-binding protein</subject><subject>Biochemistry</subject><subject>Biological Transport - drug effects</subject><subject>Biology and Life Sciences</subject><subject>Bone marrow</subject><subject>Cardiovascular disease</subject><subject>Cholesterol</subject><subject>Cholesterol - metabolism</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Dosage and administration</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - genetics</subject><subject>Drugs</subject><subject>Efflux</subject><subject>Endocrinology</subject><subject>Federal regulation</subject><subject>Female</subject><subject>Gastroenterology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - genetics</subject><subject>Gene regulation</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Hemoglobin</subject><subject>Hepatology</subject><subject>High density lipoprotein</subject><subject>Homeostasis</subject><subject>Homeostasis - drug effects</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</subject><subject>Hyperglycemia</subject><subject>Internal medicine</subject><subject>Low density lipoprotein</subject><subject>Macrophages</subject><subject>Macrophages - 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Wei-Ming</au><au>Sheu, Wayne H-H</au><au>Tseng, Pei-Chi</au><au>Lee, Tzong-Shyuan</au><au>Lee, Wen-Jane</au><au>Chang, Pey-Jium</au><au>Chiang, An-Na</au><au>Amodio, Nicola</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of microRNA Expression in Subjects with Metabolic Syndrome and Decrease of Cholesterol Efflux from Macrophages via microRNA-33-Mediated Attenuation of ATP-Binding Cassette Transporter A1 Expression by Statins</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-05-03</date><risdate>2016</risdate><volume>11</volume><issue>5</issue><spage>e0154672</spage><epage>e0154672</epage><pages>e0154672-e0154672</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Metabolic syndrome (MetS) is a complicated health problem that encompasses a variety of metabolic disorders. In this study, we analyzed the relationship between the major biochemical parameters associated with MetS and circulating levels of microRNA (miR)-33, miR-103, and miR-155. We found that miRNA-33 levels were positively correlated with levels of fasting blood glucose, glycosylated hemoglobin A1c, total cholesterol, LDL-cholesterol, and triacylglycerol, but negatively correlated with HDL-cholesterol levels. In the cellular study, miR-33 levels were increased in macrophages treated with high glucose and cholesterol-lowering drugs atorvastatin and pitavastatin. miR-33 has been reported to play an essential role in cholesterol homeostasis through ATP-binding cassette transporter A1 (ABCA1) regulation and reverse cholesterol transport. However, the molecular mechanism underlying the linkage between miR-33 and statin treatment remains unclear. In the present study, we investigated whether atorvastatin and pitavastatin exert their functions through the modulation of miR-33 and ABCA1-mediated cholesterol efflux from macrophages. The results showed that treatment of the statins up-regulated miR-33 expression, but down-regulated ABCA1 mRNA levels in RAW264.7 cells and bone marrow-derived macrophages. Statin-mediated ABCA1 regulation occurs at the post-transcriptional level through targeting of the 3'-UTR of the ABCA1 transcript by miR-33. Additionally, we found significant down-regulation of ABCA1 protein expression in macrophages treated with statins. Finally, we showed that high glucose and statin treatment significantly suppressed cholesterol efflux from macrophages. These findings have highlighted the complexity of statins, which may exert detrimental effects on metabolic abnormalities through regulation of miR-33 target genes.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27139226</pmid><doi>10.1371/journal.pone.0154672</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-05, Vol.11 (5), p.e0154672-e0154672 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1786516724 |
| 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 | 3' Untranslated regions ABC transporters ABCA1 protein Abnormalities Analysis Animals Atherosclerosis Atorvastatin ATP ATP Binding Cassette Transporter 1 - genetics ATP-binding protein Biochemistry Biological Transport - drug effects Biology and Life Sciences Bone marrow Cardiovascular disease Cholesterol Cholesterol - metabolism Complications and side effects Development and progression Diabetes Dosage and administration Down-Regulation - drug effects Down-Regulation - genetics Drugs Efflux Endocrinology Federal regulation Female Gastroenterology Gene expression Gene Expression Regulation - drug effects Gene Expression Regulation - genetics Gene regulation Genetic aspects Glucose Glucose - pharmacology Hemoglobin Hepatology High density lipoprotein Homeostasis Homeostasis - drug effects Hospitals Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Hyperglycemia Internal medicine Low density lipoprotein Macrophages Macrophages - drug effects Macrophages - metabolism Male Medicine Medicine and Health Sciences Metabolic disorders Metabolic syndrome Metabolic Syndrome - genetics Metabolic Syndrome - metabolism Metabolic syndrome X Mice MicroRNA MicroRNAs MicroRNAs - genetics Middle Aged miRNA Modulation Molecular biology Physical Sciences Physiological aspects Post-transcription Proteins RAW 264.7 Cells Ribonucleic acid RNA Statins Systemic diseases |
| title | Modulation of microRNA Expression in Subjects with Metabolic Syndrome and Decrease of Cholesterol Efflux from Macrophages via microRNA-33-Mediated Attenuation of ATP-Binding Cassette Transporter A1 Expression by Statins |
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