Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients

Abstract Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease characterized by unexplained debilitating fatigue. Although the etiology is unknown, evidence supports immunological abnormalities, such as persistent inflammation and immune-cell activation, in a subset of pat...

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Autores principales:	J. Blauensteiner, R. Bertinat, L. E. León, M. Riederer, N. Sepúlveda, F. Westermeier
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e18bf55a62e54d0b9d8f87c9f89b8829
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spelling	oai:doaj.org-article:e18bf55a62e54d0b9d8f87c9f89b88292021-12-02T14:58:53ZAltered endothelial dysfunction-related miRs in plasma from ME/CFS patients10.1038/s41598-021-89834-92045-2322https://doaj.org/article/e18bf55a62e54d0b9d8f87c9f89b88292021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-89834-9https://doaj.org/toc/2045-2322Abstract Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease characterized by unexplained debilitating fatigue. Although the etiology is unknown, evidence supports immunological abnormalities, such as persistent inflammation and immune-cell activation, in a subset of patients. Since the interplay between inflammation and vascular alterations is well-established in other diseases, endothelial dysfunction has emerged as another player in ME/CFS pathogenesis. Endothelial nitric oxide synthase (eNOS) generates nitric oxide (NO) that maintains endothelial homeostasis. eNOS is activated by silent information regulator 1 (Sirt1), an anti-inflammatory protein. Despite its relevance, no study has addressed the Sirt1/eNOS axis in ME/CFS. The interest in circulating microRNAs (miRs) as potential biomarkers in ME/CFS has increased in recent years. Accordingly, we analyze a set of miRs reported to modulate the Sirt1/eNOS axis using plasma from ME/CFS patients. Our results show that miR-21, miR-34a, miR-92a, miR-126, and miR-200c are jointly increased in ME/CFS patients compared to healthy controls. A similar finding was obtained when analyzing public miR data on peripheral blood mononuclear cells. Bioinformatics analysis shows that endothelial function-related signaling pathways are associated with these miRs, including oxidative stress and oxygen regulation. Interestingly, histone deacetylase 1, a protein responsible for epigenetic regulations, represented the most relevant node within the network. In conclusion, our study provides a basis to find endothelial dysfunction-related biomarkers and explore novel targets in ME/CFS.J. BlauensteinerR. BertinatL. E. LeónM. RiedererN. SepúlvedaF. WestermeierNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-17 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q J. Blauensteiner R. Bertinat L. E. León M. Riederer N. Sepúlveda F. Westermeier Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
description	Abstract Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease characterized by unexplained debilitating fatigue. Although the etiology is unknown, evidence supports immunological abnormalities, such as persistent inflammation and immune-cell activation, in a subset of patients. Since the interplay between inflammation and vascular alterations is well-established in other diseases, endothelial dysfunction has emerged as another player in ME/CFS pathogenesis. Endothelial nitric oxide synthase (eNOS) generates nitric oxide (NO) that maintains endothelial homeostasis. eNOS is activated by silent information regulator 1 (Sirt1), an anti-inflammatory protein. Despite its relevance, no study has addressed the Sirt1/eNOS axis in ME/CFS. The interest in circulating microRNAs (miRs) as potential biomarkers in ME/CFS has increased in recent years. Accordingly, we analyze a set of miRs reported to modulate the Sirt1/eNOS axis using plasma from ME/CFS patients. Our results show that miR-21, miR-34a, miR-92a, miR-126, and miR-200c are jointly increased in ME/CFS patients compared to healthy controls. A similar finding was obtained when analyzing public miR data on peripheral blood mononuclear cells. Bioinformatics analysis shows that endothelial function-related signaling pathways are associated with these miRs, including oxidative stress and oxygen regulation. Interestingly, histone deacetylase 1, a protein responsible for epigenetic regulations, represented the most relevant node within the network. In conclusion, our study provides a basis to find endothelial dysfunction-related biomarkers and explore novel targets in ME/CFS.
format	article
author	J. Blauensteiner R. Bertinat L. E. León M. Riederer N. Sepúlveda F. Westermeier
author_facet	J. Blauensteiner R. Bertinat L. E. León M. Riederer N. Sepúlveda F. Westermeier
author_sort	J. Blauensteiner
title	Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
title_short	Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
title_full	Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
title_fullStr	Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
title_full_unstemmed	Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients
title_sort	altered endothelial dysfunction-related mirs in plasma from me/cfs patients
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/e18bf55a62e54d0b9d8f87c9f89b8829
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Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients

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