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Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
Chronic inflammation of the adipose tissue (AT) is a major contributor to obesity-associated cardiometabolic complications. The olive oil polyphenol hydroxytyrosol (HT) contributes to Mediterranean diet cardiometabolic benefits through mechanisms still partially unknown. We investigated HT (1 and 10...
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Published in: | Nutrients 2019-10, Vol.11 (10), p.2493 |
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description | Chronic inflammation of the adipose tissue (AT) is a major contributor to obesity-associated cardiometabolic complications. The olive oil polyphenol hydroxytyrosol (HT) contributes to Mediterranean diet cardiometabolic benefits through mechanisms still partially unknown. We investigated HT (1 and 10 μmol/L) effects on gene expression (mRNA and microRNA) related to inflammation induced by 10 ng/mL tumor necrosis factor (TNF)-α in human Simpson-Golabi-Behmel Syndrome (SGBS) adipocytes. At real-time PCR, HT significantly inhibited TNF-α-induced mRNA levels, of monocyte chemoattractant protein-1, C-X-C Motif Ligand-10, interleukin (IL)-1β, IL-6, vascular endothelial growth factor, plasminogen activator inhibitor-1, cyclooxygenase-2, macrophage colony-stimulating factor, matrix metalloproteinase-2, Cu/Zn superoxide dismutase-1, and glutathione peroxidase, as well as surface expression of intercellular adhesion molecule-1, and reverted the TNF-α-mediated inhibition of endothelial nitric oxide synthase, peroxisome proliferator-activated receptor coactivator-1α, and glucose transporter-4. We found similar effects in adipocytes stimulated by macrophage-conditioned media. Accordingly, HT significantly counteracted miR-155-5p, miR-34a-5p, and let-7c-5p expression in both cells and exosomes, and prevented NF-κB activation and production of reactive oxygen species. HT can therefore modulate adipocyte gene expression profile through mechanisms involving a reduction of oxidative stress and NF-κB inhibition. By such mechanisms, HT may blunt macrophage recruitment and improve AT inflammation, preventing the deregulation of pathways involved in obesity-related diseases. |
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The olive oil polyphenol hydroxytyrosol (HT) contributes to Mediterranean diet cardiometabolic benefits through mechanisms still partially unknown. We investigated HT (1 and 10 μmol/L) effects on gene expression (mRNA and microRNA) related to inflammation induced by 10 ng/mL tumor necrosis factor (TNF)-α in human Simpson-Golabi-Behmel Syndrome (SGBS) adipocytes. At real-time PCR, HT significantly inhibited TNF-α-induced mRNA levels, of monocyte chemoattractant protein-1, C-X-C Motif Ligand-10, interleukin (IL)-1β, IL-6, vascular endothelial growth factor, plasminogen activator inhibitor-1, cyclooxygenase-2, macrophage colony-stimulating factor, matrix metalloproteinase-2, Cu/Zn superoxide dismutase-1, and glutathione peroxidase, as well as surface expression of intercellular adhesion molecule-1, and reverted the TNF-α-mediated inhibition of endothelial nitric oxide synthase, peroxisome proliferator-activated receptor coactivator-1α, and glucose transporter-4. We found similar effects in adipocytes stimulated by macrophage-conditioned media. Accordingly, HT significantly counteracted miR-155-5p, miR-34a-5p, and let-7c-5p expression in both cells and exosomes, and prevented NF-κB activation and production of reactive oxygen species. HT can therefore modulate adipocyte gene expression profile through mechanisms involving a reduction of oxidative stress and NF-κB inhibition. By such mechanisms, HT may blunt macrophage recruitment and improve AT inflammation, preventing the deregulation of pathways involved in obesity-related diseases.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu11102493</identifier><identifier>PMID: 31627295</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>adipocyte ; Adipocytes ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adipogenesis ; Angiogenesis ; Antioxidants ; Cell activation ; Cell Line ; Chemokines ; Cyclooxygenase-2 ; Diabetes ; Diet ; DNA ; Endocrinology ; Endothelial cells ; Ethanol ; exosome ; Exosomes - metabolism ; extra virgin olive oil ; Extracellular matrix ; Gelatinase A ; Gelatinase B ; Gene expression ; Gene Expression Regulation - drug effects ; Gene regulation ; Growth factors ; High fat diet ; Humans ; hydroxytyrosol ; Inflammation ; Inflammation - chemically induced ; Inflammation - metabolism ; Insulin ; insulin resistance ; Intercellular adhesion molecule 1 ; Interleukin 6 ; Lipids ; Maintenance ; Matrix metalloproteinases ; Metabolic syndrome ; Metabolites ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Obesity ; Oils & fats ; Olive oil ; Oxidative stress ; Pediatrics ; Phenylethyl Alcohol - analogs & derivatives ; Phenylethyl Alcohol - pharmacology ; Physiology ; polyphenol ; Polyphenols ; Protein Binding ; Reactive Oxygen Species ; Scavenging ; Transcription Factor RelA - metabolism ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Nutrients, 2019-10, Vol.11 (10), p.2493</ispartof><rights>2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). 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The olive oil polyphenol hydroxytyrosol (HT) contributes to Mediterranean diet cardiometabolic benefits through mechanisms still partially unknown. We investigated HT (1 and 10 μmol/L) effects on gene expression (mRNA and microRNA) related to inflammation induced by 10 ng/mL tumor necrosis factor (TNF)-α in human Simpson-Golabi-Behmel Syndrome (SGBS) adipocytes. At real-time PCR, HT significantly inhibited TNF-α-induced mRNA levels, of monocyte chemoattractant protein-1, C-X-C Motif Ligand-10, interleukin (IL)-1β, IL-6, vascular endothelial growth factor, plasminogen activator inhibitor-1, cyclooxygenase-2, macrophage colony-stimulating factor, matrix metalloproteinase-2, Cu/Zn superoxide dismutase-1, and glutathione peroxidase, as well as surface expression of intercellular adhesion molecule-1, and reverted the TNF-α-mediated inhibition of endothelial nitric oxide synthase, peroxisome proliferator-activated receptor coactivator-1α, and glucose transporter-4. We found similar effects in adipocytes stimulated by macrophage-conditioned media. Accordingly, HT significantly counteracted miR-155-5p, miR-34a-5p, and let-7c-5p expression in both cells and exosomes, and prevented NF-κB activation and production of reactive oxygen species. HT can therefore modulate adipocyte gene expression profile through mechanisms involving a reduction of oxidative stress and NF-κB inhibition. By such mechanisms, HT may blunt macrophage recruitment and improve AT inflammation, preventing the deregulation of pathways involved in obesity-related diseases.</description><subject>adipocyte</subject><subject>Adipocytes</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adipogenesis</subject><subject>Angiogenesis</subject><subject>Antioxidants</subject><subject>Cell activation</subject><subject>Cell Line</subject><subject>Chemokines</subject><subject>Cyclooxygenase-2</subject><subject>Diabetes</subject><subject>Diet</subject><subject>DNA</subject><subject>Endocrinology</subject><subject>Endothelial cells</subject><subject>Ethanol</subject><subject>exosome</subject><subject>Exosomes - metabolism</subject><subject>extra virgin olive oil</subject><subject>Extracellular matrix</subject><subject>Gelatinase A</subject><subject>Gelatinase B</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene regulation</subject><subject>Growth factors</subject><subject>High fat diet</subject><subject>Humans</subject><subject>hydroxytyrosol</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Insulin</subject><subject>insulin resistance</subject><subject>Intercellular adhesion molecule 1</subject><subject>Interleukin 6</subject><subject>Lipids</subject><subject>Maintenance</subject><subject>Matrix metalloproteinases</subject><subject>Metabolic syndrome</subject><subject>Metabolites</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Obesity</subject><subject>Oils & fats</subject><subject>Olive oil</subject><subject>Oxidative stress</subject><subject>Pediatrics</subject><subject>Phenylethyl Alcohol - analogs & derivatives</subject><subject>Phenylethyl Alcohol - pharmacology</subject><subject>Physiology</subject><subject>polyphenol</subject><subject>Polyphenols</subject><subject>Protein Binding</subject><subject>Reactive Oxygen Species</subject><subject>Scavenging</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkk1r3DAQhk1paEKaS39AMfRSCptKHlsfl8Ky5GMhTaE0h56EPsapFlvaSnaJ_3282TRNqouE5uHhZWaK4h0lpwCSfA4jpZRUtYRXxVFFeLVgrIbXz96HxUnOG7I7nHAGb4pDoKzilWyOip-Xk0vxbhqmFHPsyq_RjZ0eMJdL57fRTgOWFxiw1MGVvf9-vSzP7rYJc_YxlDfBYSrXoe103-shpqlcxeD8MBffFget7jKePN7Hxc352Y_V5eLq28V6tbxa2JpXw4KZWgABZMQ2jBtDuKGNbASgBgbScEc1cmpE61BwB5rZltDGIJXatA2B42K997qoN2qbfK_TpKL26uEjplul0-Bth0pbo2sgEoigNZFWWHCU8bYxrtaS09n1Ze_ajqZHZzEMSXcvpC8rwf9St_GPYgJYJcQs-PgoSPH3iHlQvc8Wu04HjGNWFRBOKyblLveH_9BNHFOYWzVTtKkF4bBL9GlP2Xk-OWH7FIYStVsA9W8BZvj98_hP6N9xwz0U0qtt</recordid><startdate>20191017</startdate><enddate>20191017</enddate><creator>Scoditti, Egeria</creator><creator>Carpi, Sara</creator><creator>Massaro, Marika</creator><creator>Pellegrino, Mariangela</creator><creator>Polini, Beatrice</creator><creator>Carluccio, Maria Annunziata</creator><creator>Wabitsch, Martin</creator><creator>Verri, Tiziano</creator><creator>Nieri, Paola</creator><creator>De Caterina, Raffaele</creator><general>MDPI AG</general><general>MDPI</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>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-2753-8487</orcidid><orcidid>https://orcid.org/0000-0002-3291-9009</orcidid><orcidid>https://orcid.org/0000-0001-6124-5077</orcidid></search><sort><creationdate>20191017</creationdate><title>Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition</title><author>Scoditti, Egeria ; Carpi, Sara ; Massaro, Marika ; Pellegrino, Mariangela ; Polini, Beatrice ; Carluccio, Maria Annunziata ; Wabitsch, Martin ; Verri, Tiziano ; Nieri, Paola ; De Caterina, Raffaele</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-6b48303e60c567bb07b159583ea3639b7d1ae71b8fde87d3a6cf015be19abf503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>adipocyte</topic><topic>Adipocytes</topic><topic>Adipocytes - drug effects</topic><topic>Adipocytes - metabolism</topic><topic>Adipogenesis</topic><topic>Angiogenesis</topic><topic>Antioxidants</topic><topic>Cell activation</topic><topic>Cell Line</topic><topic>Chemokines</topic><topic>Cyclooxygenase-2</topic><topic>Diabetes</topic><topic>Diet</topic><topic>DNA</topic><topic>Endocrinology</topic><topic>Endothelial cells</topic><topic>Ethanol</topic><topic>exosome</topic><topic>Exosomes - metabolism</topic><topic>extra virgin olive oil</topic><topic>Extracellular matrix</topic><topic>Gelatinase A</topic><topic>Gelatinase B</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene regulation</topic><topic>Growth factors</topic><topic>High fat diet</topic><topic>Humans</topic><topic>hydroxytyrosol</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Insulin</topic><topic>insulin resistance</topic><topic>Intercellular adhesion molecule 1</topic><topic>Interleukin 6</topic><topic>Lipids</topic><topic>Maintenance</topic><topic>Matrix metalloproteinases</topic><topic>Metabolic syndrome</topic><topic>Metabolites</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Obesity</topic><topic>Oils & fats</topic><topic>Olive oil</topic><topic>Oxidative stress</topic><topic>Pediatrics</topic><topic>Phenylethyl Alcohol - analogs & derivatives</topic><topic>Phenylethyl Alcohol - pharmacology</topic><topic>Physiology</topic><topic>polyphenol</topic><topic>Polyphenols</topic><topic>Protein Binding</topic><topic>Reactive Oxygen Species</topic><topic>Scavenging</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Scoditti, Egeria</creatorcontrib><creatorcontrib>Carpi, Sara</creatorcontrib><creatorcontrib>Massaro, Marika</creatorcontrib><creatorcontrib>Pellegrino, Mariangela</creatorcontrib><creatorcontrib>Polini, Beatrice</creatorcontrib><creatorcontrib>Carluccio, Maria Annunziata</creatorcontrib><creatorcontrib>Wabitsch, Martin</creatorcontrib><creatorcontrib>Verri, Tiziano</creatorcontrib><creatorcontrib>Nieri, Paola</creatorcontrib><creatorcontrib>De Caterina, Raffaele</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>Physical Education Index</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Scoditti, Egeria</au><au>Carpi, Sara</au><au>Massaro, Marika</au><au>Pellegrino, Mariangela</au><au>Polini, Beatrice</au><au>Carluccio, Maria Annunziata</au><au>Wabitsch, Martin</au><au>Verri, Tiziano</au><au>Nieri, Paola</au><au>De Caterina, Raffaele</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2019-10-17</date><risdate>2019</risdate><volume>11</volume><issue>10</issue><spage>2493</spage><pages>2493-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>Chronic inflammation of the adipose tissue (AT) is a major contributor to obesity-associated cardiometabolic complications. The olive oil polyphenol hydroxytyrosol (HT) contributes to Mediterranean diet cardiometabolic benefits through mechanisms still partially unknown. We investigated HT (1 and 10 μmol/L) effects on gene expression (mRNA and microRNA) related to inflammation induced by 10 ng/mL tumor necrosis factor (TNF)-α in human Simpson-Golabi-Behmel Syndrome (SGBS) adipocytes. At real-time PCR, HT significantly inhibited TNF-α-induced mRNA levels, of monocyte chemoattractant protein-1, C-X-C Motif Ligand-10, interleukin (IL)-1β, IL-6, vascular endothelial growth factor, plasminogen activator inhibitor-1, cyclooxygenase-2, macrophage colony-stimulating factor, matrix metalloproteinase-2, Cu/Zn superoxide dismutase-1, and glutathione peroxidase, as well as surface expression of intercellular adhesion molecule-1, and reverted the TNF-α-mediated inhibition of endothelial nitric oxide synthase, peroxisome proliferator-activated receptor coactivator-1α, and glucose transporter-4. We found similar effects in adipocytes stimulated by macrophage-conditioned media. Accordingly, HT significantly counteracted miR-155-5p, miR-34a-5p, and let-7c-5p expression in both cells and exosomes, and prevented NF-κB activation and production of reactive oxygen species. HT can therefore modulate adipocyte gene expression profile through mechanisms involving a reduction of oxidative stress and NF-κB inhibition. By such mechanisms, HT may blunt macrophage recruitment and improve AT inflammation, preventing the deregulation of pathways involved in obesity-related diseases.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31627295</pmid><doi>10.3390/nu11102493</doi><orcidid>https://orcid.org/0000-0003-2753-8487</orcidid><orcidid>https://orcid.org/0000-0002-3291-9009</orcidid><orcidid>https://orcid.org/0000-0001-6124-5077</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | adipocyte Adipocytes Adipocytes - drug effects Adipocytes - metabolism Adipogenesis Angiogenesis Antioxidants Cell activation Cell Line Chemokines Cyclooxygenase-2 Diabetes Diet DNA Endocrinology Endothelial cells Ethanol exosome Exosomes - metabolism extra virgin olive oil Extracellular matrix Gelatinase A Gelatinase B Gene expression Gene Expression Regulation - drug effects Gene regulation Growth factors High fat diet Humans hydroxytyrosol Inflammation Inflammation - chemically induced Inflammation - metabolism Insulin insulin resistance Intercellular adhesion molecule 1 Interleukin 6 Lipids Maintenance Matrix metalloproteinases Metabolic syndrome Metabolites MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Obesity Oils & fats Olive oil Oxidative stress Pediatrics Phenylethyl Alcohol - analogs & derivatives Phenylethyl Alcohol - pharmacology Physiology polyphenol Polyphenols Protein Binding Reactive Oxygen Species Scavenging Transcription Factor RelA - metabolism Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-TNF Tumor necrosis factor-α |
title | Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition |
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