Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro

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 ide...

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Detalles Bibliográficos
Autores: Alique, Matilde, Bodega, Guillermo, Corchete, Elena, García-Menéndez, Estefanya, Luque Pérez, Rafael, De Sequera Ortiz, Patricia, Rodríguez-Padrón, Daily, Marqués, María, Portolés, José, Carracedo Añón, Julia María, Ramírez, Rafael
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/6321
Acceso en línea:https://hdl.handle.net/20.500.14352/6321
Access Level:acceso abierto
Palabra clave:575:61
612.17
616.12
616.61
611.1.018.74
Microvesicles
Uremic toxins
Endothelial cells
Vascular cells
Calcification
Fisiología
Nefrología y urología
Sistema cardiovascular
Genética
2411 Fisiología Humana
2411.03 Fisiología Cardiovascular
2409 Genética
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oai_identifier_str oai:docta.ucm.es:20.500.14352/6321
network_acronym_str ES
network_name_str España
repository_id_str
spelling Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitroAlique, MatildeBodega, GuillermoCorchete, ElenaGarcía-Menéndez, EstefanyaLuque Pérez, RafaelDe Sequera Ortiz, PatriciaRodríguez-Padrón, DailyMarqués, MaríaPortolés, JoséCarracedo Añón, Julia MaríaRamírez, Rafael575:61612.17616.12616.61611.1.018.74MicrovesiclesUremic toxinsEndothelial cellsVascular cellsCalcificationFisiologíaNefrología y urologíaSistema cardiovascularGenética2411 Fisiología Humana2411.03 Fisiología Cardiovascular2409 GenéticaVascular 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.Computational and Structural Biotechnology JournalUniversidad Complutense de Madrid20202020-01-0120202020-01-01journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/6321reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Atribución 3.0 Españahttps://creativecommons.org/licenses/by/3.0/es/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/63212026-06-02T12:44:21Z
dc.title.none.fl_str_mv Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
title Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
spellingShingle Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
Alique, Matilde
575:61
612.17
616.12
616.61
611.1.018.74
Microvesicles
Uremic toxins
Endothelial cells
Vascular cells
Calcification
Fisiología
Nefrología y urología
Sistema cardiovascular
Genética
2411 Fisiología Humana
2411.03 Fisiología Cardiovascular
2409 Genética
title_short Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
title_full Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
title_fullStr Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
title_full_unstemmed Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
title_sort Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro
dc.creator.none.fl_str_mv Alique, Matilde
Bodega, Guillermo
Corchete, Elena
García-Menéndez, Estefanya
Luque Pérez, Rafael
De Sequera Ortiz, Patricia
Rodríguez-Padrón, Daily
Marqués, María
Portolés, José
Carracedo Añón, Julia María
Ramírez, Rafael
author Alique, Matilde
author_facet Alique, Matilde
Bodega, Guillermo
Corchete, Elena
García-Menéndez, Estefanya
Luque Pérez, Rafael
De Sequera Ortiz, Patricia
Rodríguez-Padrón, Daily
Marqués, María
Portolés, José
Carracedo Añón, Julia María
Ramírez, Rafael
author_role author
author2 Bodega, Guillermo
Corchete, Elena
García-Menéndez, Estefanya
Luque Pérez, Rafael
De Sequera Ortiz, Patricia
Rodríguez-Padrón, Daily
Marqués, María
Portolés, José
Carracedo Añón, Julia María
Ramírez, Rafael
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv 575:61
612.17
616.12
616.61
611.1.018.74
Microvesicles
Uremic toxins
Endothelial cells
Vascular cells
Calcification
Fisiología
Nefrología y urología
Sistema cardiovascular
Genética
2411 Fisiología Humana
2411.03 Fisiología Cardiovascular
2409 Genética
topic 575:61
612.17
616.12
616.61
611.1.018.74
Microvesicles
Uremic toxins
Endothelial cells
Vascular cells
Calcification
Fisiología
Nefrología y urología
Sistema cardiovascular
Genética
2411 Fisiología Humana
2411.03 Fisiología Cardiovascular
2409 Genética
description 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.
publishDate 2020
dc.date.none.fl_str_mv 2020
2020-01-01
2020
2020-01-01
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/6321
url https://hdl.handle.net/20.500.14352/6321
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 3.0 España
https://creativecommons.org/licenses/by/3.0/es/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 3.0 España
https://creativecommons.org/licenses/by/3.0/es/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Computational and Structural Biotechnology Journal
publisher.none.fl_str_mv Computational and Structural Biotechnology Journal
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15.301603

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