Notch1 modulates oxidative stress induced cell death through suppression of apoptosis signal-regulating kinase 1

Mo, Jung-Soon; Yoon, Ji-Hye; Ann, Eun-Jung; Ahn, Ji-Seon; Baek, Hyeong-Jin; Lee, Hye-Jin; Kim, Seol-Hee; Kim, Yeong‐Dae; Kim, Mi‐Yeon; Park, Hee-Sae

doi:10.1073/pnas.1209078110

Cited by 33 publications

(15 citation statements)

References 39 publications

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“…Yang et al reported that the protective effects of curcumin against oxidative stress injury (OSI) are, at least in part, dependent on Notch1 inhibition . However, it is known that, high levels of exogenous ROS upregulate Notch1 [69] which is a potent inhibitor of the oxidative stress‐induced cell death signaling pathway, resulting in positively regulation of cell survival .…”

Section: Crosstalk Between Notch and Rosmentioning

confidence: 99%

Context‐dependent function of ROS in the vascular endothelium: The role of the Notch pathway and shear stress

et al. 2017

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Reactive oxygen species (ROS) act as signal molecules in several biological processes whereas excessive, unregulated, ROS production contributes to the development of pathological conditions including endothelial dysfunction and atherosclerosis. The maintenance of a healthy endothelium depends on many factors and on their reciprocal interactions; in this framework, the Notch pathway and shear stress (SS) play two lead roles. Recently, evidence of a crosstalk between ROS, Notch, and SS, is emerging. The aim of this review is to describe the way ROS interact with the Notch pathway and SS protecting from-or promoting-the development of endothelial dysfunction. © 2017 BioFactors, 43(4):475-485, 2017.

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Section: Crosstalk Between Notch and Rosmentioning

confidence: 99%

Context‐dependent function of ROS in the vascular endothelium: The role of the Notch pathway and shear stress

et al. 2017

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“… 50 Notch1 signaling is induced by oxidative stress and Notch1 suppresses oxidative stress-induced cell death. 51 , 52 …”

Section: Discussionmentioning

confidence: 99%

COL8A2 Regulates the Fate of Corneal Endothelial Cells

Hwang

Joong

Choi

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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Purpose To investigate the effect of COL8A2 repression on corneal endothelial cells (CECs) in vitro and in vivo. Methods Cultured human CECs (hCECs) were transfected with COL8A2 siRNA ( siCOL8A2 ), and the cell viability and proliferation rate were measured. The expression of cell proliferation–associated molecules was evaluated by Western blotting and real-time reverse transcription PCR. Cell shape, Wingless-INT (WNT) signaling, and mitochondrial oxidative stress were also measured. For in vivo experiments, siCOL8A2 was transfected into rat CECs (rCECs), and corneal opacity and corneal endothelium were evaluated. Results After transfection with siCOL8A2 , COL8A2 expression was reduced (80%). Cell viability, cell proliferation rate, cyclin D1 expression, and the number of cells in the S-phase were reduced in siCOL8A2 -treated cells. The cell attained a fibroblast-like shape, and SNAI1, pSMAD2, and β-catenin expression, along with mitochondrial mass and oxidative stress levels, were altered. Corneal opacity increased, and the CECs were changed in rats in the siCOL8A2 group. Conclusions COL8A2 is required to maintain normal wound healing and CEC function.

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“…In the present study, the expression of NOTCH1 was higher in those embryos exposed to OS coupled with elevated NFE2L2 transcript, as previously has been shown (Zhao et al, ). The upregulation of NOTCH1 under high oxygen level is attributed to cell apoptosis prevention via suppression of apoptosis signal‐regulating kinase 1 ( ASK1 ), and then preventing the p38 mitogen‐activated protein kinases signaling pathway (Mo et al, ). This was more pronounced in embryos produced in vitro (Heras et al, ).…”

Section: Discussionmentioning

confidence: 99%

Sexual dimorphic expression and release of transcription factors in bovine embryos exposed to oxidative stress

Taqi

Saeed‐Zidane

Gebremedhn

et al. 2019

Molecular Reproduction Devel

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Sexually dimorphic differences in genome activity, which is orchestrated by transcription factors (TFs), could explain the differential response of male and female embryos to environmental stressors. To proof this hypothesis, the expression of cellular and extracellular TFs was investigated in male and female bovine embryos in vitro cultured either under low (5%) or high (20%) oxygen levels. The intracellular reactive oxygen species (ROS), total cell number, expression of nuclear factor (erythroid‐derived 2) factor 2 (NFE2L2), Krüppel‐like factor 4 (KLF4), notch receptor 1 (NOTCH1), E2F transcription factor 1 (E2F1), and SREBF2 along with extracellular vesicles (EVs) biogenesis genes were assessed at the blastocyst stage and their released EVs. Low blastocyst rate in both sexes due to oxidative stress (OS) was accompanied by increased ROS accumulation and reduced cell number in female embryos. The messenger RNA and protein levels of NFE2L2, as well as KLF4 expression, were higher in male embryos exposed to OS compared with female embryos. However, the expression of NOTCH1 and E2F1 was higher in female embryos cultured in high oxygen level. Male embryos exposed to OS released more EVs enriched with NFE2L2, superoxide dismutase 1, and NOTCH1 accompanied by elevated expression of EVs biogenesis genes. Accordingly, differential expression of TFs and their release into spent media could partially explain the sexual dimorphic response of bovine embryos to environmental stresses.

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Notch1 modulates oxidative stress induced cell death through suppression of apoptosis signal-regulating kinase 1

Cited by 33 publications

References 39 publications

Context‐dependent function of ROS in the vascular endothelium: The role of the Notch pathway and shear stress

Context‐dependent function of ROS in the vascular endothelium: The role of the Notch pathway and shear stress

COL8A2 Regulates the Fate of Corneal Endothelial Cells

Sexual dimorphic expression and release of transcription factors in bovine embryos exposed to oxidative stress

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