The relationship between autophagy, increased neutrophil extracellular traps formation and endothelial dysfunction in chronic kidney disease

Copyright © 2018. Published by Elsevier Inc.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 197(2018) vom: 01. Dez., Seite 189-197
Auteur principal: Kim, Jwa-Kyung (Auteur)
Autres auteurs: Park, Mi Jin, Lee, Hoi Woul, Lee, Hyung Seok, Choi, Sun Ryoung, Song, Young Rim, Kim, Hyung Jik, Park, Hyeong-Cheon, Kim, Sung Gyun
Format: Article en ligne
Langue:English
Publié: 2018
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't Autophagy Endothelial dysfunction Neutrophil extracellular traps Renal disorder Uremia Nucleosomes Leukocyte Elastase EC 3.4.21.37 plus... Tetradecanoylphorbol Acetate NI40JAQ945
Description
Résumé:Copyright © 2018. Published by Elsevier Inc.
In chronic kidney disease (CKD), the number of circulating neutrophils are increased, and this is usually accompanied by an increased basal activation state. However, the possible association between neutrophil extracellular traps (NETs) with vascular complications has not been evaluated. We assessed the relationship between NETs, autophagy and endothelial dysfunction in maintenance hemodialysis (MHD) patients. NET formation, neutrophil elastase (NE) activities, and serum nucleosome levels were measured in MHD (n = 60) and controls (n = 20). Basal NET formation were markedly increased in MHD patient compared to controls. After PMA stimulation, MHD neutrophils showed significantly increased NETs formation response than controls. The degree of NETs was strongly associated with lower flow-mediated dilatation(%) of brachial artery even after adjustment for cardiovascular risk factors and uremic toxins. Moreover, MHD neutrophils showed increased basal autophagy activity. Interestingly, the levels of NETs were markedly augmented after autophagy inhibition, suggesting a protective role of autophagy in excessive NET formation
Description:Date Completed 07.10.2019
Date Revised 07.10.2019
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2018.10.003