scholarly journals Cytosolic Guanine Nucledotide Binding Deficient Form of Transglutaminase 2 (R580a) Potentiates Cell Death in Oxygen Glucose Deprivation

PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16665 ◽  
Author(s):  
Gozde Colak ◽  
Jeffrey W. Keillor ◽  
Gail V. W. Johnson
Keyword(s):  
Cell Death ◽  
Transglutaminase 2 ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 923
Author(s):  
Yuan Yuan ◽  
Yanyu Zhai ◽  
Jingjiong Chen ◽  
Xiaofeng Xu ◽  
Hongmei Wang
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Antioxidant Capacity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Related Factor ◽  
Protective Effects

Kaempferol has been shown to protect cells against cerebral ischemia/reperfusion injury through inhibition of apoptosis. In the present study, we sought to investigate whether ferroptosis is involved in the oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal injury and the effects of kaempferol on ferroptosis in OGD/R-treated neurons. Western blot, immunofluorescence, and transmission electron microscopy were used to analyze ferroptosis, whereas cell death was detected using lactate dehydrogenase (LDH) release. We found that OGD/R attenuated SLC7A11 and glutathione peroxidase 4 (GPX4) levels as well as decreased endogenous antioxidants including nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and superoxide dismutase (SOD) in neurons. Notably, OGD/R enhanced the accumulation of lipid peroxidation, leading to the induction of ferroptosis in neurons. However, kaempferol activated nuclear factor-E2-related factor 2 (Nrf2)/SLC7A11/GPX4 signaling, augmented antioxidant capacity, and suppressed the accumulation of lipid peroxidation in OGD/R-treated neurons. Furthermore, kaempferol significantly reversed OGD/R-induced ferroptosis. Nevertheless, inhibition of Nrf2 by ML385 blocked the protective effects of kaempferol on antioxidant capacity, lipid peroxidation, and ferroptosis in OGD/R-treated neurons. These results suggest that ferroptosis may be a significant cause of cell death associated with OGD/R. Kaempferol provides protection from OGD/R-induced ferroptosis partly by activating Nrf2/SLC7A11/GPX4 signaling pathway.

scholarly journals NQO1-induced activation of AMPK contributes to cancer cell death by oxygen-glucose deprivation

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Hyemi Lee ◽  
Eun-Taex Oh ◽  
Bo-Hwa Choi ◽  
Moon-Taek Park ◽  
Ja-Kyeong Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Cancer Cell Death

scholarly journals Eye Opener in Stroke

Stroke ◽  
2019 ◽  
Vol 50 (8) ◽  
pp. 2197-2206 ◽  
Author(s):  
Hung Nguyen ◽  
Jea Young Lee ◽  
Paul R. Sanberg ◽  
Eleonora Napoli ◽  
Cesar V. Borlongan
Keyword(s):  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Glucose Deprivation ◽  
Retinal Ischemia ◽  
Artery Occlusion ◽  
Oxygen Glucose Deprivation ◽  
Retinal Pigmented Epithelium ◽  
Pigmented Epithelium ◽  
Cerebral Artery Occlusion ◽  
Epithelium Cells

Background and Purpose— Retinal ischemia is a major cause of visual impairment in stroke patients, but our incomplete understanding of its pathology may contribute to a lack of effective treatment. Here, we investigated the role of mitochondrial dysfunction in retinal ischemia and probed the potential of mesenchymal stem cells (MSCs) in mitochondrial repair under such pathological condition. Methods— In vivo, rats were subjected to middle cerebral artery occlusion then randomly treated with intravenous MSCs or vehicle. Laser Doppler was used to evaluate the blood flow in the brain and the eye, while immunohistochemical staining assessed cellular degeneration at days 3 and 14 poststroke. In vitro, retinal pigmented epithelium cells were exposed to either oxygen-glucose deprivation or oxygen-glucose deprivation and coculture with MSCs, and subsequently, cell death and mitochondrial function were examined immunocytochemically and with Seahorse analyzer, respectively. Results— Middle cerebral artery occlusion significantly reduced blood flow in the brain and the eye accompanied by mitochondrial dysfunction and ganglion cell death at days 3 and 14 poststroke. Intravenous MSCs elicited mitochondrial repair and improved ganglion cell survival at day 14 poststroke. Oxygen-glucose deprivation similarly induced mitochondrial dysfunction and cell death in retinal pigmented epithelium cells; coculture with MSCs restored mitochondrial respiration, mitochondrial network morphology, and mitochondrial dynamics, which likely attenuated oxygen-glucose deprivation-mediated retinal pigmented epithelium cell death. Conclusions— Retinal ischemia is closely associated with mitochondrial dysfunction, which can be remedied by stem cell-mediated mitochondrial repair.

Down-modulation of Bis sensitizes cell death in C6 glioma cells induced by oxygen–glucose deprivation

2010 ◽  
Vol 1349 ◽  
pp. 1-10 ◽  
Author(s):  
Seung Eun Jung ◽  
Yong Kwan Kim ◽  
Dong-Ye Youn ◽  
Mi-Hyun Lim ◽  
Jeong Heon Ko ◽  
...  
Keyword(s):  
Cell Death ◽  
Glioma Cells ◽  
Glucose Deprivation ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Oxygen Glucose Deprivation

scholarly journals Silencing of Long Noncoding RNA Nespas Aggravates Microglial Cell Death and Neuroinflammation in Ischemic Stroke

Stroke ◽  
2019 ◽  
Vol 50 (7) ◽  
pp. 1850-1858 ◽  
Author(s):  
Yiming Deng ◽  
Duanduan Chen ◽  
Luyao Wang ◽  
Feng Gao ◽  
Bo Jin ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Noncoding Rnas ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Oxygen Glucose Deprivation ◽  
Cerebral Artery Occlusion

Background and Purpose— Ischemic stroke is one of the leading causes of morbidity and mortality worldwide and a major cause of long-term disability. Recently, long noncoding RNAs have been revealed, which are tightly associated with several human diseases. However, the functions of long noncoding RNAs in ischemic stroke still remain largely unknown. In the current study, for the first time, we investigated the role of long noncoding RNA Nespas in ischemic stroke. Methods— We used in vivo models of middle cerebral artery occlusion and in vitro models of oxygen-glucose deprivation to illustrate the effect of long noncoding RNA Nespas on ischemic stroke. Results— We found expression of Nespas was significantly increased in ischemic cerebral tissues and oxygen-glucose deprivation–treated BV2 cells in a time-dependent manner. Silencing of Nespas aggravated middle cerebral artery occlusion operation–induced IR injury and cell death. In addition, proinflammatory cytokine production and NF-κB (nuclear factor-κB) signaling activation were inhibited by Nespas overexpression. TAK1 (transforming growth factor-β–activated kinase 1) was found to directly interact with Nespas, and TAK1 activation was significantly suppressed by Nespas. At last, we found Nespas-inhibited TRIM8 (tripartite motif 8)-induced K63-linked polyubiquitination of TAK1. Conclusions— We showed that Nespas played anti-inflammatory and antiapoptotic roles in cultured microglial cells after oxygen-glucose deprivation stimulation and in mice after ischemic stroke by inhibiting TRIM8-related K63-linked polyubiquitination of TAK1.

scholarly journals P2X7 receptor activation regulates microglial cell death during oxygen-glucose deprivation

2013 ◽  
Vol 73 ◽  
pp. 311-319 ◽  
Author(s):  
Ukpong B. Eyo ◽  
Sam A. Miner ◽  
Katelin E. Ahlers ◽  
Long-Jun Wu ◽  
Michael E. Dailey
Keyword(s):  
Cell Death ◽  
P2x7 Receptor ◽  
Microglial Cell ◽  
Glucose Deprivation ◽  
Receptor Activation ◽  
Oxygen Glucose Deprivation ◽  
P2x7 Receptor Activation
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