کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8287318 | 1535839 | 2017 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tert-butyl hydroperoxide (t-BHP) induced apoptosis and necroptosis in endothelial cells: Roles of NOX4 and mitochondrion
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کلمات کلیدی
N-acetyl-l-cysteinenecrosulfonamideTTFAMLKLnecrostatin-1RIP3RIP1antimycin Ac-Jun-N-terminal kinaseNOX4NSAASK1DCFH2-DADPIERKNACJnkMMPXanthine oxidase - زانتین اکسیداز2-Thenoyltrifluoroacetone - 2-تداویلتری فلوئوراکتون3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide - 3- (4،5-dimethyl-2-thiazolyl) -2،5-difenyl-2-H-tetrazolium bromideMAPKs - MAPK هاMTT - MTTNADPH oxidase 4 - NADPH اکسیداز 4Nec-1 - NEC-1ROS - ROSt-BHP - T-BHPz-VAD-fmk - Z-VAD-FMKHydrogen peroxide - آب اکسیژنهallopurinol - آلوپورینولApoptosis - خزان یاختهایDiphenyleneiodonium - دیفنیلن اندونیمRot - روتRotenone - روتنونEndothelial cells - سلولهای اندوتلیالextracellular signal regulated kinase - سیگنال خارج سلولی kinase را تنظیم می کندMitochondria - میتوکندریاNecroptosis - نئروپتوزیسALL - همهtert-butyl hydroperoxide - هیدروپراکسید تری بوتیلH2O2 - هیدروژن پراکسیدMitochondrial membrane potential - پتانسیل غشای میتوکندریreceptor-interacting protein 1 - پروتئین تعامل گیرنده 1mixed lineage kinase domain-like protein - پروتئین مشابه پروتئین کیناز لینوکسی مخلوطPropidium iodide - پروتئین یدیدmitogen-activated protein kinases - کیناز پروتئین فعال MitogenReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Oxidative stress causes endothelial death while underlying mechanisms remain elusive. Herein, the pro-death effect of tert-butyl hydroperoxide (t-BHP) was investigated with low concentration (50 μM) of t-BHP (t-BHPL) and high concentration (500 μM) of t-BHP (t-BHPH). Both t-BHPL and t-BHPH induced endothelial cell death was determined. T-BHPL induced caspase-dependent apoptosis and reactive oxygen species (ROS) generation, which was inhibited by N-acetyl-L-cysteine (NAC). Furthermore, NADPH oxidase inhibitor diphenyleneiodonium (DPI), NOX4 siRNA, and NOX4 inhibitor GKT137831 reduced t-BHPL-induced ROS generation while mitochondrial respiratory chain inhibitors rotenone (Rot), 2-thenoyltrifluoroacetone (TTFA), and antimycin A (AA) failed to do so. NOX4 overexpression resulted in increased ROS generation and Akt expression but decreased sensitivity to t-BHPL. In contrast, T-BHPH induced LDH release, PI uptake, and cell translucent cytoplasm. RIP1 inhibitor necrostatin-1 (Nec-1), MLKL inhibitor necrosulfonamide (NSA) and silencing RIP1, RIP3, and MLKL inhibited t-BHPH-induced cell death while pan-caspase inhibitor Z-VAD-FMK showed no effect. T-BHPH-induced ROS production was inhibited by TTFA, AA and Rot while DPI showed no effect. T-BHPH induced RIP1/RIP3 interaction, which was decreased by Rot, TTFA, and AA. Silence RIP1 and RIP3 but not MLKL inhibited t-BHPH-induced mitochondrial membrane potential (MMP) decrease and ROS production. Moreover, P38MAPK inhibitor SB203580 reversed both t-BHPL and t-BHPH-induced cell death while inhibitors for ERKs and JNKs showed no obvious effect. These data suggested that t-BHP induced both apoptosis and necroptosis in endothelial cells which was mediated by ROS and p38MAPK. ROS derived from NADPH oxidase and mitochondria contributed to t-BHPL and t-BHPH-induced apoptosis and necroptosis, respectively.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Redox Biology - Volume 11, April 2017, Pages 524-534
Journal: Redox Biology - Volume 11, April 2017, Pages 524-534
نویسندگان
Wenwen Zhao, Haitao Feng, Wen Sun, Kang Liu, Jin-Jian Lu, Xiuping Chen,