ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite‐induced apoptosis of NB4 cells

Li, Zhushi; Shi, Kejian; Guan, Lina; Cao, Tingming; Jiang, Qian; Yang, Yang; Xu, Caimin

doi:10.1016/j.febslet.2010.03.040

Cited by 60 publications

(61 citation statements)

References 46 publications

(54 reference statements)

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“…Accumulating evidences confirmed the application of selenite in studies of cell proliferation and cancer (3,4). Previous results suggested supranutritional doses of selenite promoted cell death through mitochondria-or ER stress-mediated apoptotic pathway in human leukemia cell lines (5,6). Furthermore, autophagy has recently been considered as an alternative mechanism of cell death induced by selenite, which caused concurrence of autophagy and apoptosis in leukemia cells (7,8).…”

Section: Introductionmentioning

confidence: 78%

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Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Jiang

Li²,

Shi³

et al. 2012

BMB Reports

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Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at Ser 308. We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at Ser 308 serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise. [BMB reports 2012; 45(3): [194][195][196][197][198][199]

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Section: Introductionmentioning

confidence: 78%

“…Previous studies indicated that the antitumor activity of selenium compounds was often attributed to drug-induced apoptosis (5,6,20). Here we addressed that autophagy acted as another essential mechanism for the application of selenite in cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Jiang

Li²,

Shi³

et al. 2012

BMB Reports

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“…We have also shown that the level of ROS is maintained to its sub-lethal concentration by upregulation of SOD-1. This can be correlated with a feedback response related to increasing in ROS production by cristacarpin, which eventually maintains the sub-lethal concentration of ROS essential for senescence (Li et al 2010). The detailed mechanism is under investigation of our laboratory.…”

Section: Discussionmentioning

confidence: 94%

Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21waf-1

Chakraborty

Rasool

Kumar

et al. 2016

AGE

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Stress-induced premature senescence (SIPS) is quite similar to replicative senescence that is committed by cells exposed to various stress conditions viz. ultraviolet radiation (DNA damage), hydrogen peroxide (oxidative stress), chemotherapeutic agents (cytotoxic threat), etc. Here, we report that cristacarpin, a natural product obtained from the stem bark of Erythrina suberosa, promotes endoplasmic reticulum (ER) stress, leading to sub-lethal reactive oxygen species (ROS) generation and which eventually terminates by triggering senescence in pancreatic and breast cancer cells through blocking the cell cycle in the G1 phase. The majority of cristacarpin-treated cells responded to conventional SA-β-gal stains; showed characteristic p21 waf1 upregulation along with enlarged and flattened morphology; and increased volume, granularity, and formation of heterochromatin foci-all of these features are the hallmarks of senescence. Inhibition of ROS generation by N-acetyl-L-cysteine (NAC) significantly reduced the expression of p21 waf1 , confirming that the modulation in p21 waf1 by anti-proliferative cristacarpin was ROS dependent. Further, the elevation in p21 waf1 expression in PANC-1 and MCF-7 cells was consistent with the decrease in the expression of Cdk-2 and cyclinD1. Here, we provide evidence that cristacarpin promotes senescence in a p53-independent manner. Moreover, cristacarpin treatment induced p38MAPK, indicating the ROS-dependent activation of the MAP kinase pathway, and thus abrogates the tumor growth in mouse allograft tumor model.

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“…Detection of Reactive Oxygen Species (ROS) ROS generation by VSMCs was measured with ROS assay kit (Beyotime, China) according to the manufacturer's instruction. 19) In brief, VSMCs were cultured in 6-well plates and synchronized by DMEM without serum overnight. VSMCs were treated with 100 µM naringenin for 30 min and then exposed to 1 µM angiotensin II for 1 h. Cells were then incubated with 10 µM 2,′7′-dichlorodihydrofluorescein diacetate (DCFH-DA) for 30 min in dark at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Naringenin Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cells Proliferation and Migration and Decreases Neointimal Hyperplasia in Balloon Injured Rat Carotid Arteries through Suppressing Oxidative Stress

Chen

Zhang

et al. 2013

Biological & Pharmaceutical Bulletin

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Proliferation and migration of vascular smooth muscle cells (VSMCs) play pivotal roles in the development of restenosis after angioplasty and oxidative stress involves both processes. Naringenin, a flavanone compound found in citrus fruits, has been widely evaluated for antioxidant activity. This study was designed to explore whether naringenin could inhibit angiotensin II-induced VSMCs proliferation and migration and decrease neointimal hyperplasia in balloon injured rat carotid arteries. VSMCs were treated with or without naringenin before stimulation with 1 µM angiotensin II and twenty-four rats were subjected to carotid arteries injury and the carotid arteries were harvested at 14 d after balloon injury. The results showed naringenin led to a significant inhibition of angiotensin II-induced VSMCs proliferation and migration. Naringenin significantly attenuated the reactive oxygen species production, increased the superoxide dismutase activity and decreased the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, reduced phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) and the nuclear translocation of nuclear factor (NF)-κB p65 in angiotensin II-treated VSMCs. Moreover, naringenin decreased the ratio of neointima to media by 63.8% in balloon injured rat carotid arteries, and the serum level of 8-iso-prostaglandin F2α in naringenin-treated rats was significantly decreased. These results indicated naringenin exhibited antioxidant activity on angiotensin II-treated VSMCs and balloon injured rat carotid arteries and could be a potential protective agent for restenosis after angioplasty.Key words naringenin; vascular smooth muscle cell; oxidative stress; neointimal hyperplasia; angiotensin II Coronary heart disease (CHD) remains the leading cause of mortality in most developed countries and many developing countries.1,2) Percutaneous coronary intervention with or without intracoronary stent placement is widely used for treatment of symptomatic CHD and has greatly improved the survival rate.3,4) However, restenosis after angioplasty, which happen in 5-10% patients, is still a major clinical problem. 5,6) Studies have shown that abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) play pivotal roles in the development of restenosis after angioplasty, as well as in atherosclerosis.7-9) Inhibition of proliferation and migration of VSMCs could remarkably attenuate the neointimal hyperplasia in animal studies. 10-12)Naringenin, a flavanone compound found in citrus fruits, such as oranges and grapes, 13) has been pharmacologically evaluated for antioxidant activity.14,15) Although some studies showed that naringenin could inhibit VSMCs proliferation and migration in vitro, 16,17) the effect and mechanism of naringenin on vascular injury are still far from clear. In this investigation, we attempted to evaluate whether naringenin could inhibit angiotensin II-induced VSMCs proliferation and migration in vitro a...

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ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite‐induced apoptosis of NB4 cells

Cited by 60 publications

References 46 publications

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Sodium selenite-induced activation of DAPK promotes autophagy in human leukemia HL60 cells

Cristacarpin promotes ER stress-mediated ROS generation leading to premature senescence by activation of p21waf-1

Naringenin Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cells Proliferation and Migration and Decreases Neointimal Hyperplasia in Balloon Injured Rat Carotid Arteries through Suppressing Oxidative Stress

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