CIKS (Act1 or TRAF3IP2) mediates Angiotensin-II-induced Interleukin-18 expression, and Nox2-dependent cardiomyocyte hypertrophy

Article ID	Journal	Published Year	Pages	File Type
10953926	Journal of Molecular and Cellular Cardiology	2012	12 Pages	PDF

Abstract

âº Ang-II induces cardiomyocyte hypertrophy and fibrosis via CIKS. âº Ang-II induces CIKS expression via AT1/Nox2-mediated ROS generation. âº Ang-II enhances CIKS binding to IKKÎ² and JNK. âº CIKS acts as a scaffold in IKKÎ³/JNK interaction. âº CIKS is a potential therapeutic target in cardiac hypertrophy and adverse remodeling.

Keywords

Janus Kinase 2 NEMO IκB RAAS JAK2 Rac1 DPI PLC dichlorofluorescein AT1 IKK ANF IRF TAK1 AP-1 TRAF GLP TRAF3IP2 CIKS Act1 SAPK c-jun amino-terminal kinase ATRAP TNF Rho-associated, coiled-coil containing protein kinase 1 UTR EMSA GFP CREB NF-κB MMP Jnk Dcf SBP NADPH GST SEF DCFH-DA ACM C/EBP IκB kinase MOI NOx ROS Electrophoretic mobility shift assay angiotensin II type 1 receptor Oct NADPH oxidase interleukin TIR diphenylene iodonium Ras-related C3 botulinum toxin substrate 1 renin–angiotensin–aldosterone system IFN regulatory factor TNF receptor associated factor dominant negative atrial natriuretic factor tumor necrosis factor nuclear factor kappa B phospholipase C systolic blood pressure Fibrosis matrix metalloproteinase NF-κB essential modulator untranslated region inhibitory κB wild-type nicotinamide adenine dinucleotide phosphate Cardiac hypertrophy CCAAT/enhancer-binding protein activator protein-1 green fluorescent protein cAMP response element-binding protein Stress-activated protein kinase multiplicity of infection Adult cardiomyocytes glutathione-S-transferase Reactive oxygen species Rock