Fig 7.tif (561.71 kB)
CLIC1 promotes adhesion of monocytes to and inflammation of ECs under oxidative stress.
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posted on 2016-11-18, 17:41 authored by Yingling Xu, Ji Zhu, Xiao Hu, Cui Wang, Dezhao Lu, Chenxue Gong, Jinhuan Yang, Lei ZongCont group: HUVECs with normal culture medium for 12h. H2O2 group: HUVECs with H2O2 exposure for 12h. IAA94 group: HUVECs with 40μM IAA94 pretreatment for 1 h and then H2O2 exposure for 12h. CLIC1-/- group: CLIC1-/- HUVECs with H2O2 exposure for 12h. (A) and (B) The pro-inflammatory cytokines IL-1β (A) and TNF-α (B) levels determined by ELISA both were increased after H2O2 exposure, whereas IAA94 and CLIC1 deficiency markedly obstructed their increase. (C) and (D) IAA94 and CLIC1 deficiency obviously reduced ICAM-1 and VCAM-1 relative expression levels at the protein level. *P < 0.05, **P < 0.01 versus Cont group, #P < 0.05, ##P < 0.01 versus H2O2 group. Error bars represent SD of three replicate experiments.
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CLIC 1 Inhibition Attenuates Vascular Inflammationatherosclerotic plaque developmentIAAOverexpressed CLIC 1CLIC 1cytoplasmic chloride ion concentrationCLIC 1 translocationROSICAMcell membraneSuppressing CLIC 1 expressionMDAIntracellular chloride channel 1oxidative stressH 2 O 2oxidative damagechloride-selective ion channelsHUVECVCAMCLIC 1 expressionApolipoprotein E-deficient miceinhibitor indanyloxyacetic acid -94SOD enzyme activityCLIC 1 membrane translocationASTNFILEndothelial Injury Endothelial dysfunction
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