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Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition
In chronic kidney disease (CKD), hyperphosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal and vascular injury, and TNFα-induction of neutral-sphingomyelinase2 (nSMase2) to release p...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6882851/ https://www.ncbi.nlm.nih.gov/pubmed/31780737 http://dx.doi.org/10.1038/s41598-019-54306-8 |
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author | Arcidiacono, Maria Vittoria Carrillo-López, Natalia Panizo, Sara Castro-Grattoni, Anabel L. Valcheva, Petya Ulloa, Catalina Rodríguez-Carrio, Javier Cardús, Anna Quirós-Caso, Covadonga Martínez-Arias, Laura Martínez-Salgado, Carlos Motilva, María José Rodriguez-Suarez, Carmen Cannata-Andía, Jorge B. Dusso, Adriana S. |
author_facet | Arcidiacono, Maria Vittoria Carrillo-López, Natalia Panizo, Sara Castro-Grattoni, Anabel L. Valcheva, Petya Ulloa, Catalina Rodríguez-Carrio, Javier Cardús, Anna Quirós-Caso, Covadonga Martínez-Arias, Laura Martínez-Salgado, Carlos Motilva, María José Rodriguez-Suarez, Carmen Cannata-Andía, Jorge B. Dusso, Adriana S. |
author_sort | Arcidiacono, Maria Vittoria |
collection | PubMed |
description | In chronic kidney disease (CKD), hyperphosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal and vascular injury, and TNFα-induction of neutral-sphingomyelinase2 (nSMase2) to release pro-calcifying exosomes. This study examined anti-inflammatory β-glucans efficacy at attenuating systemic inflammation in health, and renal and vascular injury favoring VC in hyperphosphatemic CKD. In healthy adults, dietary barley β-glucans (Bβglucans) reduced leukocyte superoxide production, inflammatory ADAM17, TNFα, nSMase2, and pro-aging/pro-inflammatory STING (Stimulator of interferon genes) gene expression without decreasing circulating inflammatory cytokines, except for γ-interferon. In hyperphosphatemic rat CKD, dietary Bβglucans reduced renal and aortic ADAM17-driven inflammation attenuating CKD-progression (higher GFR and lower serum creatinine, proteinuria, kidney inflammatory infiltration and nSMase2), and TNFα-driven increases in aortic nSMase2 and calcium deposition without improving mineral homeostasis. In VSMC, Bβglucans prevented LPS- or uremic serum-induced rapid increases in ADAM17, TNFα and nSMase2, and reduced the 13-fold higher calcium deposition induced by prolonged calcifying conditions by inhibiting osteogenic differentiation and increases in nSMase2 through Dectin1-independent actions involving Bβglucans internalization. Thus, dietary Bβglucans inhibit leukocyte superoxide production and leukocyte, renal and aortic ADAM17- and nSMase2 gene expression attenuating systemic inflammation in health, and renal injury and aortic calcification despite hyperphosphatemia in CKD. |
format | Online Article Text |
id | pubmed-6882851 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-68828512019-12-06 Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition Arcidiacono, Maria Vittoria Carrillo-López, Natalia Panizo, Sara Castro-Grattoni, Anabel L. Valcheva, Petya Ulloa, Catalina Rodríguez-Carrio, Javier Cardús, Anna Quirós-Caso, Covadonga Martínez-Arias, Laura Martínez-Salgado, Carlos Motilva, María José Rodriguez-Suarez, Carmen Cannata-Andía, Jorge B. Dusso, Adriana S. Sci Rep Article In chronic kidney disease (CKD), hyperphosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal and vascular injury, and TNFα-induction of neutral-sphingomyelinase2 (nSMase2) to release pro-calcifying exosomes. This study examined anti-inflammatory β-glucans efficacy at attenuating systemic inflammation in health, and renal and vascular injury favoring VC in hyperphosphatemic CKD. In healthy adults, dietary barley β-glucans (Bβglucans) reduced leukocyte superoxide production, inflammatory ADAM17, TNFα, nSMase2, and pro-aging/pro-inflammatory STING (Stimulator of interferon genes) gene expression without decreasing circulating inflammatory cytokines, except for γ-interferon. In hyperphosphatemic rat CKD, dietary Bβglucans reduced renal and aortic ADAM17-driven inflammation attenuating CKD-progression (higher GFR and lower serum creatinine, proteinuria, kidney inflammatory infiltration and nSMase2), and TNFα-driven increases in aortic nSMase2 and calcium deposition without improving mineral homeostasis. In VSMC, Bβglucans prevented LPS- or uremic serum-induced rapid increases in ADAM17, TNFα and nSMase2, and reduced the 13-fold higher calcium deposition induced by prolonged calcifying conditions by inhibiting osteogenic differentiation and increases in nSMase2 through Dectin1-independent actions involving Bβglucans internalization. Thus, dietary Bβglucans inhibit leukocyte superoxide production and leukocyte, renal and aortic ADAM17- and nSMase2 gene expression attenuating systemic inflammation in health, and renal injury and aortic calcification despite hyperphosphatemia in CKD. Nature Publishing Group UK 2019-11-28 /pmc/articles/PMC6882851/ /pubmed/31780737 http://dx.doi.org/10.1038/s41598-019-54306-8 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Arcidiacono, Maria Vittoria Carrillo-López, Natalia Panizo, Sara Castro-Grattoni, Anabel L. Valcheva, Petya Ulloa, Catalina Rodríguez-Carrio, Javier Cardús, Anna Quirós-Caso, Covadonga Martínez-Arias, Laura Martínez-Salgado, Carlos Motilva, María José Rodriguez-Suarez, Carmen Cannata-Andía, Jorge B. Dusso, Adriana S. Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition |
title | Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition |
title_full | Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition |
title_fullStr | Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition |
title_full_unstemmed | Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition |
title_short | Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition |
title_sort | barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through adam17 and neutral-sphingomyelinase2 inhibition |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6882851/ https://www.ncbi.nlm.nih.gov/pubmed/31780737 http://dx.doi.org/10.1038/s41598-019-54306-8 |
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