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


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Alique, Matilde and Bodega, Guillermo and Corchete, Elena and García-Menéndez, Estefanya and Sequera, Patricia de and Luque, Rafael and Rodríguez-Padrón, Daily and Marqués, María and Portolés, José and Carracedo Añón, Julia María and Ramírez, Rafael (2020) Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification in vitro. pp. 953-966. ISSN ESSN: 2001-0370 (In Press)

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Official URL: https://www.sciencedirect.com/science/article/pii/S2001037020300295


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.

Item Type:Article
Uncontrolled Keywords:Microvesicles; Uremic toxins; Endothelial cells; Vascular cells; Calcification
Subjects:Medical sciences > Medicine > Physiology
Medical sciences > Medicine > Nephrology and Urology
Medical sciences > Medicine > Cardiovascular system
Medical sciences > Biology > Genetics
ID Code:60869
Deposited On:12 Jun 2020 09:17
Last Modified:12 Jun 2020 11:47

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