scholarly journals Bid-mediated mitochondrial damage is a key mechanism in glutamate-induced oxidative stress and AIF-dependent cell death in immortalized HT-22 hippocampal neurons

2010 ◽  
Vol 18 (2) ◽  
pp. 282-292 ◽  
Author(s):  
S Tobaben ◽  
J Grohm ◽  
A Seiler ◽  
M Conrad ◽  
N Plesnila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Hippocampal Neurons ◽  
Mitochondrial Damage ◽  
Dependent Cell

scholarly journals Blockage of NOX2/MAPK/NF-κB Pathway Protects Photoreceptors against Glucose Deprivation-Induced Cell Death

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Bin Fan ◽  
Bei-Fen Wang ◽  
Lin Che ◽  
Ying-Jian Sun ◽  
Shu-Yan Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Western Blot ◽  
Glucose Deprivation ◽  
Photoreceptor Cells ◽  
Retinal Neurons ◽  
Dependent Cell ◽  
Ischemic Diseases ◽  
Cell Death Cascade ◽  
Energy Failure

Acute energy failure is one of the critical factors contributing to the pathogenic mechanisms of retinal ischemia. Our previous study demonstrated that glucose deprivation can lead to a caspase-dependent cell death of photoreceptors. The aim of this study was to decipher the upstream signal pathway in glucose deprivation- (GD-) induced cell death. We mimicked acute energy failure by using glucose deprivation in photoreceptor cells (661W cells). GD-induced oxidative stress was evaluated by measuring ROS with the DCFH-DA assay and HO-1 expression by Western blot analysis. The activation of NOX2/MAPK/NF-κB signal was assessed by Western blot and immunohistochemical assays. The roles of these signals in GD-induced cell death were measured by using their specific inhibitors. Inhibition of Rac-1 and NOX2 suppressed GD-induced oxidative stress and protected photoreceptors against GD-induced cell death. NOX2 was an upstream signal in the caspase-dependent cell death cascade, yet the downstream MAPK pathways were activated and blocking MAPK signals rescued 661W cells from GD-induced death. In addition, GD caused the activation of NF-κB signal and inhibiting NF-κB significantly protected 661W cells. These observations may provide insights for treating retinal ischemic diseases and protecting retinal neurons from ischemia-induced cell death.

scholarly journals Screening for Lung Cancer with Low Dose Computed Tomography (LDCT)

2021 ◽  
pp. 794-832
Author(s):  
Elena Locci ◽  
Silvia Raymond
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Research Team ◽  
Low Dose ◽  
Small Cell ◽  
Small Cell Lung ◽  
Tumor Cell Death ◽  
Dependent Cell ◽  
Keywords Cancer ◽  
Low Dose Computed Tomography

Using samples of small cell lung tumors, a research team led by biologist Dr. Raymond discovered two new ways to induce tumor cell death. By activating ferroptosis, one of two subtypes of tumor cells can be targeted: first, iron-dependent cell death due to oxidative stress, and second, oxidative stress. Therefore, cell death can also be induced in a different way. Both types of cell death must be caused by drugs at the same time to eliminate the majority of the tumor mass. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

scholarly journals Role of CNC1 gene in TDP-43 aggregation-induced oxidative stress-mediated cell death in S. cerevisiae model of ALS

2020 ◽  
Author(s):  
Vidhya Bharathi ◽  
Amandeep Girdhar ◽  
Basant K Patel
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Stress Response ◽  
Molecular Mechanisms ◽  
Motor Neuron Diseases ◽  
C Protein ◽  
Cell Death Pathway ◽  
Cyclin C ◽  
Dependent Cell ◽  
Anti Oxidant

ABSTRACTTDP-43 is a multi-functional ribonucleoprotein that is also found deposited as hyper-phosphorylated and ubiquitinated TDP-43 inclusions in the brain and spinal cord of the patients of the motor neuron diseases, amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Till date, how the cell death ensues is not fully deciphered although several molecular mechanisms of the TDP-43 toxicity such as impairments of endocytosis and chromatin remodelling, mis-regulations of autophagy and proteasome function, mis-localization to the mitochondria and generation of oxidative stress etc., have been proposed. A predominantly nuclear protein, Cyclin C, can regulate the oxidative stress response by affecting the transcription of stress response genes and also by translocation to the cytoplasm for the activation of the mitochondrial fragmentation-dependent cell death pathway. Using the well-established yeast model of TDP-43 aggregation and toxicity, we examined here whether upon TDP-43 aggregation, the cell survival depends on the presence of the CNC1 gene that encodes Cyclin C protein or other genes that encode proteins that function in conjunction with Cyclin C, such as the DNM1, FIS1 and MED13 genes. We found that the TDP-43 toxicity is significantly reduced in the yeast deleted for the CNC1 or DNM1 genes. Importantly, the rescue of TDP-43 toxicity in these yeast deletion backgrounds required the presence of functional mitochondria. Also, the deletion of YBH3 gene, which encodes for a protein involved in the mitochondria-dependent apoptosis, also reduced the TDP-43 toxicity. Furthermore, Cyclin C-YFP was observed to localize from the nucleus to the cytoplasm in response to the TDP-43 co-expression. Also, this cytoplasmic localization of Cyclin C was prevented by the addition of an anti-oxidant molecule, N-acetyl-cysteine. Taken together, our data suggest that Cyclin C, Dnm1 and Ybh3 proteins are important in mediating the TDP-43-induced oxidative stress-mediated cell death in the S. cerevisiae model.

scholarly journals Presenilin 1 Regulates [Ca2+]i and Mitochondria/ER Interaction in Cultured Rat Hippocampal Neurons

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Eduard Korkotian ◽  
Anna Meshcheriakova ◽  
Menahem Segal
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Survival Rate ◽  
Hippocampal Neurons ◽  
Presenilin 1 ◽  
Abrupt Increase ◽  
Lower Survival Rate ◽  
Neuronal Functions ◽  
Mushroom Spines

Mutations in the presenilin 1 (PS1) gene are a major trigger of familial Alzheimer’s disease (AD), yet the mechanisms affected by mutated PS1 causing cognitive decline are not yet elucidated. In the present study, we compared rat hippocampal neurons in culture, transfected with PS1 or with mutant (M146V) PS1 (mPS1) plasmids in several neuronal functions. Initially, we confirmed earlier observations that mPS1-expressing neurons are endowed with fewer mature “mushroom” spines and more filopodial immature protrusions. The correlation between calcium changes in the cytosol, mitochondria, and endoplasmic reticulum (ER) is mitigated in the mPS1 neurons, tested by the response to an abrupt increase in ambient [Ca2+]o; cytosolic [Ca2+]i is higher in the mPS1 neurons but mitochondrial [Ca2+] is lower than in control neurons. Strikingly, mPS1-transfected neurons express higher excitability and eventual lower survival rate when exposed to the oxidative stressor, paraquat. These results highlight an impaired calcium regulation in mPS1 neurons, resulting in a reduced ability to handle oxidative stress, which may lead to cell death and AD.

scholarly journals Increased Uptake of Zinc in Malignant Cells is Associated with Enhanced Activation of MAPK Signalling and P53-Dependent Cell Injury

2008 ◽  
Vol 51 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Emil Rudolf
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Injury ◽  
Cell Damage ◽  
Zinc Homeostasis ◽  
Malignant Cells ◽  
Intracellular Zinc ◽  
Free Zinc ◽  
Dependent Cell ◽  
Zinc Levels

Excess intracellular zinc has been demonstrated to be responsible for cell injury and cell death in various experimental as well as clinical models. While the cells possess a system of mechanisms regulating intracellular zinc homeostasis, their saturation by acutely increased zinc levels or by a sustained exposure to elevated zinc levels results in liberation of free zinc stores within the cells and ultimate cell damage and cell death. Here we report that in Hep-2 malignant cells enhanced uptake of zinc causes activation of mitogen-activated protein kinase (MAPK) signaling with resulting p53-dependent cell injury which can be significantly prevented by specific p53 inhibition and by prevention of oxidative stress. Our observations are consistent with the view that subacutely increased intracellular free zinc levels stimulate via oxidative stress p53-dependent pathways which are responsible for the final cell damage in tumor cells.

17-beta estradiol inhibits oxidative stress-induced accumulation of AIF into nucleolus and PARP1-dependent cell death via estrogen receptor alpha

2015 ◽  
Vol 232 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Enkhzaya Batnasan ◽  
Ruoxi Wang ◽  
Jitao Wen ◽  
Yueshuang Ke ◽  
Xiaoxue Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Receptor Alpha ◽  
Dependent Cell

scholarly journals Investigation of the Impact of Low–Dose Computed Tomography (LDCT) Screening for Primary Lung Cancer (PLC) on the Risk of Developing Brain Metastasis (BM) after Primary Lung Cancer (PLC) Diagnosis

2021 ◽  
pp. 782-824
Author(s):  
Ricardo Gobato ◽  
Abhijit Mitra
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cell Death ◽  
Low Dose ◽  
Primary Lung Cancer ◽  
Tumor Cell Death ◽  
Dependent Cell ◽  
Keywords Cancer ◽  
Low Dose Computed Tomography ◽  
The Impact

Using samples of small cell lung tumors, a research team led by biologist Dr. Raymond discovered two new ways to induce tumor cell death. By activating ferroptosis, one of two subtypes of tumor cells can be targeted: first, iron-dependent cell death due to oxidative stress, and second, oxidative stress. Therefore, cell death can also be induced in a different way. Both types of cell death must be caused by drugs at the same time to eliminate the majority of the tumor mass. Keywords: Cancer; Cells; Tissues; Tumors; Prevention; Prognosis; Diagnosis; Imaging; Screening, Treatment; Management

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