Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification

Calcification Endothelial cells Microvesicles Uremic toxins Vascular cells

Journal

Computational and structural biotechnology journal
ISSN: 2001-0370
Titre abrégé: Comput Struct Biotechnol J
Pays: Netherlands
ID NLM: 101585369

Informations de publication

Date de publication:
2020
Historique:
received: 24 01 2020
revised: 02 04 2020
accepted: 05 04 2020
entrez: 6 5 2020
pubmed: 6 5 2020
medline: 6 5 2020
Statut: epublish

Résumé

Vascular calcification (VC), an unpredictable pathophysiological process and critical event in patients with cardiovascular diseases (CVDs), is the leading cause of morbi-mortality and disability in chronic kidney disease (CKD) patients worldwide. Currently, no diagnostic method is available for identifying patients at risk of VC development; the pathology is detected when the process is irreversible. Extracellular vesicles (EVs) from endothelial cells might promote VC. Therefore, their evaluation and characterization could be useful for designing new diagnostic tools. The aim of the present study is to investigate whether microvesicles (MVs) from endothelial cells damaged by uremic toxin and indoxyl sulfate (IS) could induce calcification in human vascular smooth muscle cells (VMSCs). Besides, we have also analyzed the molecular mechanisms by which these endothelial MVs can promote VC development. Endothelial damage has been evaluated according to the percentage of senescence in endothelial cells, differential microRNAs in endothelial cells, and the amount of MVs released per cell. To identify the role of MVs in VC, VSMCs were treated with MVs from IS-treated endothelial cells. Calcium, inflammatory gene expression, and procalcification mediator levels in VSMCs were determined. IS-treated endothelial cells underwent senescence and exhibited modulated microRNA expression and an increase in the release of MVs. VSMCs exposed to these MVs modulated the expression of pro-inflammatory genes and some mediators involved in calcification progression. MVs produced by IS-treated endothelial cells promoted calcification in VSMCs.

Identifiants

pubmed: 32368330
doi: 10.1016/j.csbj.2020.04.006
pii: S2001-0370(20)30029-5
pmc: PMC7184105
doi:

Types de publication

Journal Article

Langues

eng

Pagination

953-966

Informations de copyright

© 2020 The Authors.

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Auteurs

Matilde Alique (M)

Departamento de Biología de Sistemas, Universidad de Alcalá (IRYCIS), Alcalá de Henares, Madrid, Spain.

Guillermo Bodega (G)

Departamento de Biomedicina y Biotecnología, Universidad de Alcalá, Alcalá de Henares, Madrid, Spain.

Elena Corchete (E)

Sección de Nefrología, Hospital Universitario Infanta Leonor, Madrid, Spain.

Estefanya García-Menéndez (E)

Servicio Nefrología, Hospital Universitario Puerta de Hierro, Madrid, Spain.

Patricia de Sequera (P)

Sección de Nefrología, Hospital Universitario Infanta Leonor, Madrid, Spain.

Rafael Luque (R)

Departamento de Química Orgánica, Universidad de Córdoba, Edificio Marie Curie (C-3), Carretera Nacional IV-A, Km 396, Córdoba, Spain.

Daily Rodríguez-Padrón (D)

Departamento de Química Orgánica, Universidad de Córdoba, Edificio Marie Curie (C-3), Carretera Nacional IV-A, Km 396, Córdoba, Spain.

María Marqués (M)

Servicio Nefrología, Hospital Universitario Puerta de Hierro, Madrid, Spain.

José Portolés (J)

Servicio Nefrología, Hospital Universitario Puerta de Hierro, Madrid, Spain.

Julia Carracedo (J)

Departamento de Genética, Fisiología y Microbiología, Facultad de Ciencias Biológicas, Universidad Complutense de Madrid/ Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain.

Rafael Ramírez (R)

Departamento de Biología de Sistemas, Universidad de Alcalá (IRYCIS), Alcalá de Henares, Madrid, Spain.

Classifications MeSH