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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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Autores principales: Scoditti, Egeria, Carpi, Sara, Massaro, Marika, Pellegrino, Mariangela, Polini, Beatrice, Carluccio, Maria Annunziata, Wabitsch, Martin, Verri, Tiziano, Nieri, Paola, De Caterina, Raffaele
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836288/
https://www.ncbi.nlm.nih.gov/pubmed/31627295
http://dx.doi.org/10.3390/nu11102493
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author Scoditti, Egeria
Carpi, Sara
Massaro, Marika
Pellegrino, Mariangela
Polini, Beatrice
Carluccio, Maria Annunziata
Wabitsch, Martin
Verri, Tiziano
Nieri, Paola
De Caterina, Raffaele
author_facet Scoditti, Egeria
Carpi, Sara
Massaro, Marika
Pellegrino, Mariangela
Polini, Beatrice
Carluccio, Maria Annunziata
Wabitsch, Martin
Verri, Tiziano
Nieri, Paola
De Caterina, Raffaele
author_sort Scoditti, Egeria
collection PubMed
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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spelling pubmed-68362882019-11-21 Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition Scoditti, Egeria Carpi, Sara Massaro, Marika Pellegrino, Mariangela Polini, Beatrice Carluccio, Maria Annunziata Wabitsch, Martin Verri, Tiziano Nieri, Paola De Caterina, Raffaele Nutrients Article 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. MDPI 2019-10-17 /pmc/articles/PMC6836288/ /pubmed/31627295 http://dx.doi.org/10.3390/nu11102493 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Scoditti, Egeria
Carpi, Sara
Massaro, Marika
Pellegrino, Mariangela
Polini, Beatrice
Carluccio, Maria Annunziata
Wabitsch, Martin
Verri, Tiziano
Nieri, Paola
De Caterina, Raffaele
Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
title Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
title_full Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
title_fullStr Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
title_full_unstemmed Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
title_short Hydroxytyrosol Modulates Adipocyte Gene and miRNA Expression Under Inflammatory Condition
title_sort hydroxytyrosol modulates adipocyte gene and mirna expression under inflammatory condition
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6836288/
https://www.ncbi.nlm.nih.gov/pubmed/31627295
http://dx.doi.org/10.3390/nu11102493
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