IL-17 induces apoptosis of vascular endothelial cells : a potential mechanism for human acute coronary syndrome

Copyright © 2011 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 141(2011), 2 vom: 15. Nov., Seite 152-60
1. Verfasser: Zhu, Faliang (VerfasserIn)
Weitere Verfasser: Wang, Qun, Guo, Chun, Wang, Xiaoyan, Cao, Xuelei, Shi, Yongyu, Gao, Fei, Ma, Chunhong, Zhang, Lining
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2011
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Comparative Study Journal Article Research Support, Non-U.S. Gov't BAX protein, human IL17A protein, human IL6 protein, human Interleukin-17 Interleukin-6 Proto-Oncogene Proteins c-bcl-2 Recombinant Proteins mehr... Transforming Growth Factor beta bcl-2-Associated X Protein von Willebrand Factor CASP3 protein, human EC 3.4.22.- CASP9 protein, human Caspase 3 Caspase 9
Beschreibung
Zusammenfassung:Copyright © 2011 Elsevier Inc. All rights reserved.
Th17 cells producing IL-17 are involved in the pathogenesis of atherosclerosis, but the underlying mechanisms remain unclear. In this study, we investigated the effects of IL-17 on human vascular endothelial cells and showed that IL-17 induced cell death of the vascular endothelial cells, which played a pivotal role in plaque destabilization triggering acute coronary syndrome (ACS). We showed that circulating Th17 cells and IL-17 increased in patients with ACS compared to the patients with stable angina or health individuals; the plasma levels of IL-6 increased but TGF-β decreased in ACS patients, exhibiting a positive and negative correlation with that of IL-17, respectively. Importantly, we uncovered that IL-17 promoted the production of von Willebrand factor by endothelial cells and induced endothelial apoptosis by activating caspase-3, caspase-9 and up-regulating the ratio of Bax/Bcl-2, indicating the function of IL-17 in vascular endothelial damage as a potential mechanism for the pathogenesis of human ACS
Beschreibung:Date Completed 20.12.2011
Date Revised 10.04.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2011.07.003