Secretory activity of the coronary artery endothelial cells in conditions of the peritoneal dialysis

Misian, Monika; Baum, Ewa; Bręborowicz, Andrzej

doi:10.1080/0886022x.2021.2023024

Cited by 2 publications

(1 citation statement)

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“…Comprehensive analysis of common and differential molecular alterations induced by the different available PD fluids and their specific properties has been extensively conducted in mesothelial cells but is missing for endothelial cells [ 5 , 9 , 10 , 11 , 12 , 13 ]. In endothelial cells, only a few selected individual parameters have been analyzed following PD fluid exposure, but a holistic untargeted analysis to decipher molecular changes has not been performed [ 5 , 14 , 15 , 16 , 17 ]. As it is not feasible to perform repeated peritoneal biopsies in chronic PD patients, experimental models must be utilized to study these chronic vessel changes and their molecular perturbations associated with PD within the peritoneal membrane.…”

Section: Introductionmentioning

confidence: 99%

Proteome-Wide Differential Effects of Peritoneal Dialysis Fluid Properties in an In Vitro Human Endothelial Cell Model

Sacnun

Hoogenboom

Eibensteiner

et al. 2022

IJMS

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To replace kidney function, peritoneal dialysis (PD) utilizes hyperosmotic PD fluids with specific physico-chemical properties. Their composition induces progressive damage of the peritoneum, leading to vasculopathies, decline of membrane function, and PD technique failure. Clinically used PD fluids differ in their composition but still remain bioincompatible. We mapped the molecular pathomechanisms in human endothelial cells induced by the different characteristics of widely used PD fluids by proteomics. Of 7894 identified proteins, 3871 were regulated at least by 1 and 49 by all tested PD fluids. The latter subset was enriched for cell junction-associated proteins. The different PD fluids individually perturbed proteins commonly related to cell stress, survival, and immune function pathways. Modeling two major bioincompatibility factors of PD fluids, acidosis, and glucose degradation products (GDPs) revealed distinct effects on endothelial cell function and regulation of cellular stress responses. Proteins and pathways most strongly affected were members of the oxidative stress response. Addition of the antioxidant and cytoprotective additive, alanyl-glutamine (AlaGln), to PD fluids led to upregulation of thioredoxin reductase-1, an antioxidant protein, potentially explaining the cytoprotective effect of AlaGln. In conclusion, we mapped out the molecular response of endothelial cells to PD fluids, and provided new evidence for their specific pathomechanisms, crucial for improvement of PD therapies.

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