NLRP3 inflammasome mediates angiotension II-induced expression of inflammatory factor interleukin-1β in human umbilical vein endothelial cells.
- Author:
Ren-Qiang YANG
1
;
Ling HUANG
;
Xiao-Xin MA
;
Si-Yi JIN
;
Dan WANG
;
Xu LI
Author Information
- Publication Type:Journal Article
- MeSH: Adaptor Proteins, Signal Transducing; pharmacology; Angiotensin II; pharmacology; Blotting, Western; Carrier Proteins; metabolism; Caspase 1; metabolism; Human Umbilical Vein Endothelial Cells; metabolism; Humans; Hydrogen Peroxide; Inflammasomes; metabolism; Interleukin-1beta; metabolism; NADPH Oxidase 4; NADPH Oxidases; metabolism; NLR Family, Pyrin Domain-Containing 3 Protein; RNA, Small Interfering; Reactive Oxygen Species; metabolism
- From: Journal of Southern Medical University 2016;36(6):790-795
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of angiotension II (AngII) on the activation of NLRP3 inflammasome and the expression of interleukin-1β (IL-1β) in human umbilical vein endothelial cells (HUVECs).
METHODSHUVECs cultured in vitro were treated with different concentrations of AngII for varying lengths of time to determine the optimal concentration and time for AngII exposure. To test the impact of different agents on the effect of AngII exposure, HUVECs were pretreated with AngII receptor blocker losartan, NAD(P)H inhibitor DPI and H(2)O(2) scavenger CAT, caspase 1 inhibitor YVAD, or NLRP3 siRNA for silencing NLRP3, and the protein levels of NOX4, NLRP3, caspase-1 and IL-1β in HUVECs were analyzed by Western blotting.
RESULTSAngII treatment at the optimal concentration (10(-9) mol/L) for 12 h significantly increased the protein levels of NOX4, NLRP3, caspase1 and IL-1β in HUVECs. Pretreatment with losartan, DPI, CAT, YVAD, or NLRP3 siRNA all attenuated the effects of AngII on the cells.
CONCLUSIONAngII can induce vascular inflammation by promoting the production of reactive oxygen species and activating NLRP3 inflammasome to increase the protein expression of IL-1β in HUVECs.
