کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8268979 | 1534956 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
c-Jun N-terminal kinase attenuates TNFα signaling by reducing Nox1-dependent endosomal ROS production in vascular smooth muscle cells
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کلمات کلیدی
NF-κBreduced nicotinamide-adenine dinucleotide phosphateTMHERKNADPHeGFPESRJnkc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKNOx - NOXROS - ROSsiRNA - siRNAsmall interfering ribonucleic acid - اسید ریبونوکلئیک دخالت کندNADPH oxidase - اکسیداز NADPH Electron spin resonance - رزونانس اسپین الکترونNuclear factor-kappa B - فاکتور هسته ای-کاپا BASK - پرسیدنenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیapoptosis signal-regulating kinase - کیناز تنظیم کننده سیگنال آپوپتوزReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: c-Jun N-terminal kinase attenuates TNFα signaling by reducing Nox1-dependent endosomal ROS production in vascular smooth muscle cells c-Jun N-terminal kinase attenuates TNFα signaling by reducing Nox1-dependent endosomal ROS production in vascular smooth muscle cells](/preview/png/8268979.png)
چکیده انگلیسی
Tumor necrosis factor-α (TNFα), a proinflammatory cytokine, causes vascular smooth muscle cell (VSMC) proliferation and migration and promotes inflammatory vascular lesions. Nuclear factor-kappa B (NF-κB) activation by TNFα requires endosomal superoxide production by Nox1. In endothelial cells, TNFα stimulates c-Jun N-terminal kinase (JNK), which inhibits NF-κB signaling. The mechanism by which JNK negatively regulates TNFα-induced NF-κB activation has not been defined. We hypothesized that JNK modulates NF-κB activation in VSMC, and does so via a Nox1-dependent mechanism. TNFα-induced NF-κB activation was TNFR1- and endocytosis-dependent. Inhibition of endocytosis with dominant-negative dynamin (DynK44A) potentiated TNFα-induced JNK activation, but decreased ERK activation, while p38 kinase phosphorylation was not altered. DynK44A attenuated intracellular, endosomal superoxide production in wild-type (WT) VSMC, but not in NADPH oxidase 1 (Nox1) knockout (KO) cells. siRNA targeting JNK1 or JNK2 potentiated, while a JNK activator (anisomycin) inhibited, TNFα-induced NF-κB activation in WT, but not in Nox1 KO cells. TNFα-stimulated superoxide generation was enhanced by JNK1 inhibition in WT, but not in Nox1 KO VSMC. These data suggest that JNK suppresses the inflammatory response to TNFα by reducing Nox1-dependent endosomal ROS production. JNK and endosomal superoxide may represent novel targets for pharmacologic modulation of TNFα signaling and vascular inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 86, September 2015, Pages 219-227
Journal: Free Radical Biology and Medicine - Volume 86, September 2015, Pages 219-227
نویسندگان
Hyehun Choi, Anna Dikalova, Ryan J. Stark, Fred S. Lamb,