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

Authors
 Jwa-Kyung Kim  ;  Mi Jin Park  ;  Hoi Woul Lee  ;  Hyung Seok Lee  ;  Sun Ryoung Choi  ;  Young Rim Song  ;  Hyung Jik Kim  ;  Hyeong-Cheon Park  ;  Sung Gyun Kim 
Citation
 Clinical Immunology, Vol.197 : 189-197, 2018 
Journal Title
 Clinical Immunology 
ISSN
 1521-6616 
Issue Date
2018
Keywords
Autophagy ; Endothelial dysfunction ; Neutrophil extracellular traps ; Renal disorder ; Uremia
Abstract
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.
Full Text
https://www.sciencedirect.com/science/article/pii/S1521661618304649
DOI
10.1016/j.clim.2018.10.003
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Park, Hyeong Cheon(박형천) ORCID logo https://orcid.org/0000-0002-1550-0812
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/165927
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