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https://www.readbyqxmd.com/read/28440498/differentiation-of-human-induced-pluripotent-stem-cells-in-william-s-e-initiation-medium-supplemented-with-3%C3%A2-bromopyruvate-and-2%C3%A2-deoxy%C3%A2-d%C3%A2-glucose
#1
Minoru Tomizawa, Fuminobu Shinozaki, Yasufumi Motoyoshi, Takao Sugiyama, Shigenori Yamamoto, Naoki Ishige
Hepatocyte selection medium (HSM) is deprived of glucose and supplemented with galactose, and is based on Leibovitz's‑15 (L15) medium. HSM may promote the differentiation of human induced pluripotent stem (iPS) cells towards hepatocyte lineage. These culture conditions result in increased expression of galactokinase (GALK)‑1 and GALK2. However, iPS cells do not survive in HSM. Two potential alternatives to glucose deprivation are treatment with 3‑bromopyruvate (3BP), an analogue of pyruvate, and 2‑deoxy‑d‑glucose (2DG), an analogue of glucose...
April 12, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28438530/ferulic-acid-attenuates-brain-microvascular-endothelial-cells-damage-caused-by-oxygen-glucose-deprivation-via-punctate-mitochondria-dependent-mitophagy
#2
Jun-Li Chen, Wen-Jun Duan, Si Luo, Shi Li, Xiao-Hui Ma, Bo-Nan Hou, Shu-Yi Cheng, Shu-Huan Fang, Qi Wang, Shui-Qing Huang, Yun-Bo Chen
Ferulic acid (FA) has an important effect on scavenging free radicals, which is related to the alleviation of various neurodegenerative diseases. However, there are few studies about its effects on vascular dementia. In this study, we demonstrated the effect of FA on oxidative damage of brain microvascular endothelial cells (BMECs) which underwent oxygen-glucose deprivation (OGD) for 2 hours. Our data showed that FA significantly reversed the oxidative stress state of OGD-treated BMECs and reduced mitochondrial dysfunction...
April 21, 2017: Brain Research
https://www.readbyqxmd.com/read/28436948/mitochondrial-elongation-mediated-glucose-metabolism-reprogramming-is-essential-for-tumour-cell-survival-during-energy-stress
#3
J Li, Q Huang, X Long, X Guo, X Sun, X Jin, Z Li, T Ren, P Yuan, X Huang, H Zhang, J Xing
To date, mechanisms of tumour cell survival under energy stress are not well understood. Cumulative evidence is beginning to reveal that specific mitochondrial morphologies are often associated with energetic states and survival of cells. However, the functional roles of mitochondria in the metabolic adaptation of tumour cells to energy stress remain to be elucidated. In this study, we first investigated the changes in mitochondrial morphology induced by nutrition deprivation in tumour cells, and the underlying molecular mechanism...
April 24, 2017: Oncogene
https://www.readbyqxmd.com/read/28433662/iron-and-thiol-redox-signaling-in-cancer-an-exquisite-balance-to-escape-ferroptosis
#4
REVIEW
Shinya Toyokuni, Fumiya Ito, Kyoko Yamashita, Yasumasa Okazaki, Shinya Akatsuka
Epidemiological data indicate a constant worldwide increase in cancer mortality, although the age of onset is increasing. Recent accumulation of genomic data on human cancer via next-generation sequencing confirmed that cancer is a disease of genome alteration. In many cancers, the Nrf2 transcription system is activated via mutations either in Nrf2 or Keap1 ubiquitin ligase, leading to persistent activation of the genes with antioxidative functions. Furthermore, deep sequencing of passenger mutations is clarifying responsible cancer causative agent(s) in each case, including aging, APOBEC activation, smoking and UV...
April 19, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28433650/long-noncoding-rna-malat1-is-a-potent-autophagy-inducer-protecting-brain-microvascular-endothelial-cells-against-oxygen-glucose-deprivation-reoxygenation-induced-injure-by-sponing-mir-26b-and-upregulating-ulk2-expression
#5
Zhijun Li, Jing Li, Na Tang
Brain microvascular endothelial cell (BMEC) injury induced by ischemia-reperfusion (I/R) is the initial stage of blood-brain barrier (BBB) disruption, which results in a poor prognosis in ischemic stroke patients. Autophagy has been shown to have protective effects on BMECs against cerebral ischemic insults. However, molecular mechanism of BMEC autophagy during I/R is unclear. Long noncoding RNAs (lncRNAs) are emerging as new factors involved in cell autophagy. LncRNA Malat1 is one of the most highly upregulated I/R or OGD/R-responsive endothelial lncRNA and plays a protective role in BMECs against cerebral ischemic insults...
April 19, 2017: Neuroscience
https://www.readbyqxmd.com/read/28430666/myc-induced-glutaminolysis-bypasses-hif-driven-glycolysis-in-hypoxic-small-cell-lung-carcinoma-cells
#6
Matilda Munksgaard Thorén, Marica Vaapil, Johan Staaf, Maria Planck, Martin E Johansson, Sofie Mohlin, Sven Påhlman
We previously demonstrated that small cell lung carcinoma (SCLC) cells lack HIF-2α protein expression, whereas HIF-1α in these cells is expressed at both acute and prolonged hypoxia. Here we show that low HIF2A expression correlates with high expression of MYC genes. Knockdown of HIF1A expression had no or limited effect on cell survival and growth in vitro. Unexpectedly, hypoxic ATP levels were not affected by HIF-1α knockdown and SCLC cell viability did not decrease upon glucose deprivation. In line with these in vitro data, xenograft tumor-take and growth were not significantly affected by repressed HIF1A expression...
April 6, 2017: Oncotarget
https://www.readbyqxmd.com/read/28424784/evaluation-of-connexin-43-redistribution-and-endocytosis-in-astrocytes-subjected-to-ischemia-reperfusion-or-oxygen-glucose-deprivation-and-reoxygenation
#7
Hongyan Xie, Yu Cui, Shuai Hou, Juan Wang, Jing Miao, Fang Deng, Jiachun Feng
Connexin 43 (Cx43) is the major component protein in astrocytic gap junction communication. Recent studies have shown the cellular processes of gap junction internalization and degradation, but many details remain unknown. This study investigated the distribution of Cx43 and its mechanism after ischemic insult. Astrocyte culture system and a model of ischemia/reperfusion (IR) or oxygen-glucose deprivation and reoxygenation (OGDR) were established. Cx43 distribution was observed by laser scanning confocal microscopy under different cultivation conditions...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28424593/phospholipase-a2-of-peroxiredoxin-6-plays-a-critical-role-in-cerebral-ischemia-reperfusion-inflammatory-injury
#8
Yu Shanshan, Jiang Beibei, Tan Li, Gao Minna, Lei Shipeng, Peng Li, Zhao Yong
Microglia-mediated inflammation is an important step in the progression of cerebral ischemia/reperfusion injury and the associated production of receptors of immunomoudulation, including Toll-like receptors (TLRs). Peroxiredoxin 6 (Prdx6) has been demonstrated as the endogenous antioxidant protein for its peroxidase properties. However, the role of the independent phospholipase A2 (iPLA2) activity of Prdx6 in stroke has not been well studied. In this study, we evaluated whether blocking the calcium-iPLA2 activity of Prdx6 using siRNA and inhibitors (1-hexadecyl-3-(trifluoroethgl)-sn-glycerol-2 phosphomethanol, MJ33) would have a critical effect on inflammatory brain damage...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28424584/hif-1%C3%AE-overexpression-improves-transplanted-bone-mesenchymal-stem-cells-survival-in-rat-mcao-stroke-model
#9
Bingke Lv, Feng Li, Jianbang Han, Jie Fang, Limin Xu, Chengmei Sun, Tian Hua, Zhongfei Zhang, Zhiming Feng, Xiaodan Jiang
Bone mesenchymal stem cells (BMSCs) death after transplantation is a serious obstacle impacting on the outcome of cell therapy for cerebral infarction. This study was aimed to investigate whether modification of BMSCs with hypoxia-inducible factor 1α (Hif-1α) could enhance the survival of the implanted BMSCs. BMSCs were isolated from Wistar rats, and were infected with Hif-1α-GFP lentiviral vector or Hif-1α siRNA. The modified BMSCs were exposed to oxygen-glucose deprivation (OGD) condition, cellular viability and apoptosis were then assessed...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28424420/vitexin-protects-against-hypoxic-ischemic-injury-via-inhibiting-ca2-calmodulin-dependent-protein-kinase-ii-and-apoptosis-signaling-in-the-neonatal-mouse-brain
#10
Jia-Wei Min, Wei-Lin Kong, Song Han, Nageeb Bsoul, Wan-Hong Liu, Xiao-Hua He, Russell M Sanchez, Bi-Wen Peng
Neonatal hypoxic-ischemic is a major cause of death and disability in neonates. In this study, we suggest for the first time that pretreatment with vitexin may suppress a pro-apoptotic signaling pathway in hypoxic-ischemic neuronal injury in neonates by inhibition of the phosphorylation of Ca2+/Calmodulin-dependent protein kinase II. Here we found that vitexin pretreatment reduced brain infarct volume in a dose-dependent manner. In addition, vitexin decreased the number of TUNEL-positive cells and brain atrophy...
April 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28421304/increased-autophagic-degradation-contributes-to-the-neuroprotection-of-hydrogen-sulfide-against-cerebral-ischemia-reperfusion-injury
#11
Yuanjun Zhu, Mengyang Shui, Xiaoyan Liu, Wenhui Hu, Yinye Wang
Hydrogen sulfide (H2S), an endogenous gaseous signal molecule, exhibits protective effect against ischemic injury. However, its underlying mechanism is not fully understood. We have recently reported that exogenous H2S decreases the accumulation of autophagic vacuoles in mouse brain with ischemia/reperfusion (I/R) injury. To further investigate whether this H2S-induced reduction of autophagic vacuoles is caused by the decreased autophagosome synthesis and/or the increased autophagic degradation inautophagic flux, we performed in vitro and in vivo studies using SH-SY5Y cells for the oxygen and glucose deprivation/reoxygenation (OGD/R) and mice for the cerebral I/R, respectively...
April 18, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/28414075/vitamin-b2-deficiency-enhances-the-pro-inflammatory-activity-of-adipocyte-consequences-for-insulin-resistance-and-metabolic-syndrome-development
#12
Agnieszka Irena Mazur-Bialy, Ewa Pocheć
AIMS: Adipose tissue is an endocrine organ important for regulation of such physiological processes as energy metabolism or lipids homeostasis. In an obesity state, it participates in the induction of chronic systemic inflammation accompanied by pro-inflammatory cytokines and fatty acid elevation. For this reasons, adipose tissue is involved in, e.g., insulin resistance, type 2 diabetes or hyperlipidemia development. In our previous study, we have shown that riboflavin deficiency induces a pathological pro-inflammatory response of macrophages, the main component of adipose tissue...
April 14, 2017: Life Sciences
https://www.readbyqxmd.com/read/28413477/isoquercetin-activates-the-erk1-2-nrf2-pathway-and-protects-against-cerebral-ischemia-reperfusion-injury-in-vivo-and-in-vitro
#13
Miao Chen, Li-Hua Dai, Aihua Fei, Shu-Ming Pan, Hai-Rong Wang
Isoquercetin has exhibited a wide range of therapeutic properties, including antioxidant, anti-inflammatory and anti-allergic activities. The aim of the present study was to investigate the effect of isoquercetin on rats with 2 h middle cerebral artery occlusion (MCAO) and evaluate the neuroprotective effect of isoquercetin on a primary culture of rat hippocampal neuronal cells subjected to oxygen-glucose deprivation followed by reoxygenation (OGD/R). In vivo, the rats treated with isoquercetin exhibited a lower degree of neurological dysfunction and smaller infarct volume than the vehicle-treated rats...
April 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28413461/long-noncoding-rna-malat1-inhibits-apoptosis-induced-by-oxygen-glucose-deprivation-and-reoxygenation-in-human-brain-microvascular-endothelial-cells
#14
Jia-Wei Xin, Yu-Gang Jiang
Cerebral ischemia/reperfusion (I/R) injury leads to brain vascular dysfunction, which is characterized by endothelial cell injury or death. Long noncoding (lnc) RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is reportedly associated with endothelial cell functions and dysfunctions. In the present study, the role of MALAT1 in I/R-induced cerebral vascular endothelial cell apoptosis was explored using oxygen-glucose deprivation and reoxygenation (OGD-R) as an in vitro I/R injury model. Primary human brain microvascular endothelial cells were cultured under OGD-R, and the expression levels of MALAT1 and cell apoptosis were measured at 6, 9, 12, 24 and 36 h post-reoxygenation...
April 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28412735/glucose-deprivation-elicits-phenotypic-plasticity-via-zeb1-mediated-expression-of-nnmt
#15
Justyna Kanska, Paul-Joseph P Aspuria, Barbie Taylor-Harding, Lindsay Spurka, Vincent Funari, Sandra Orsulic, Beth Y Karlan, W Ruprecht Wiedemeyer
Glucose is considered the primary energy source for all cells, and some cancers are addicted to glucose. Here, we investigated the functional consequences of chronic glucose deprivation in serous ovarian cancer cells. We found that cells resistant to glucose starvation (glucose-restricted cells) demonstrated increased metabolic plasticity that was dependent on NNMT (Nicotinamide N-methyltransferase) expression. We further show that ZEB1 induced NNMT, rendered cells resistant to glucose deprivation and recapitulated metabolic adaptations and mesenchymal gene expression observed in glucose-restricted cells...
February 17, 2017: Oncotarget
https://www.readbyqxmd.com/read/28411585/the-association-between-air-pollution-and-type-2-diabetes-in-a-large-cross-sectional-study-in-leicester-the-champions-study
#16
Gary O'Donovan, Yogini Chudasama, Samuel Grocock, Roland Leigh, Alice M Dalton, Laura J Gray, Thomas Yates, Charlotte Edwardson, Sian Hill, Joe Henson, David Webb, Kamlesh Khunti, Melanie J Davies, Andrew P Jones, Danielle H Bodicoat, Alan Wells
BACKGROUND: Observational evidence suggests there is an association between air pollution and type 2 diabetes; however, there is high risk of bias. OBJECTIVE: To investigate the association between air pollution and type 2 diabetes, while reducing bias due to exposure assessment, outcome assessment, and confounder assessment. METHODS: Data were collected from 10,443 participants in three diabetes screening studies in Leicestershire, UK. Exposure assessment included standard, prevailing estimates of outdoor nitrogen dioxide and particulate matter concentrations in a 1×1km area at the participant's home postcode...
April 12, 2017: Environment International
https://www.readbyqxmd.com/read/28411102/zl006-protects-spinal-cord-neurons-against-ischemia-induced-oxidative-stress-through-ampk-pgc-1%C3%AE-sirt3-pathway
#17
Shu-Guang Liu, Yun-Mei Wang, Yan-Jun Zhang, Xi-Jing He, Tao Ma, Wei Song, Yu-Min Zhang
Spinal cord ischemia (SCI) induces a range of cellular and molecular cascades, including activation of glutamate receptors and downstream signaling. Post-synaptic density protein 95 (PSD-95) links neuronal nitric oxide synthase (nNOS) with the N-methyl-d-aspartic acid (NMDA) receptors to form a ternary complex in the CNS. This molecular complex-mediated cytotoxicity has been implicated in brain ischemia, but its role in SCI has not been determined. The goal of the study was to investigate the potential protective effects of ZL006, a small-molecule inhibitor of the PSD-95/nNOS interaction, in an in vitro SCI model induced by oxygen and glucose deprivation (OGD) in cultured spinal cord neurons...
April 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28405935/4-chlorodiazepam-protects-mitochondria-in-t98g-astrocyte-cell-line-from-glucose-deprivation
#18
Eliana Baez, Gina Paola Guio-Vega, Valentina Echeverria, Daniel Andres Sandoval-Rueda, George E Barreto
The translocator protein (TSPO), formerly known as the peripheral-type benzodiazepine receptor (PBR), is considered an important regulator of steroidogenesis and a potential therapeutic target in neurological disorders. Previous evidence suggests that TSPO ligands can protect cells during injury and prevent apoptosis in central nervous system (CNS) cells. However, its actions on astrocytic cells under metabolic injury are not well understood. In this study, we explored whether 4'-chlorodiazepam (Ro5-4864), a TSPO ligand, might protect astrocyte mitochondria under glucose deprivation...
April 13, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28402151/tanshinone-inhibits-neuronal-cell-apoptosis-and-inflammatory-response-in-cerebral-infarction-rat-model
#19
Liang Zhou, Jie Zhang, Chao Wang, Qiangsan Sun
We aimed to investigate the effect and mechanisms of tanshinone (TSN) IIA in cerebral infarction. The cerebral infarction rat model was established by middle cerebral artery occlusion (MCAO). After pretreatment with TSN, cerebral infarct volume, cerebral edema, and neurological deficits score were evaluated, as well as cell apoptosis in hippocampus and cortex of the brain was examined with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) were determined by Enzyme-Linked Immunosorbent Assay (ELISA)...
April 1, 2017: International Journal of Immunopathology and Pharmacology
https://www.readbyqxmd.com/read/28400812/edaravone-protects-against-oxygen-glucose-serum-deprivation-restoration-induced-apoptosis-in-spinal-cord-astrocytes-by-inhibiting-integrated-stress-response
#20
Bin Dai, Ting Yan, Yi-Xing Shen, You-Jia Xu, Hai-Bin Shen, Dong Chen, Jin-Rong Wang, Shuang-Hua He, Qi-Rong Dong, Ai-Liang Zhang
We previously found that oxygen-glucose-serum deprivation/restoration (OGSD/R) induces apoptosis of spinal cord astrocytes, possibly via caspase-12 and the integrated stress response, which involves protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor 2-alpha (eIF2α) and activating transcription factor 4 (ATF4). We hypothesized that edaravone, a low molecular weight, lipophilic free radical scavenger, would reduce OGSD/R-induced apoptosis of spinal cord astrocytes. To test this, we established primary cultures of rat astrocytes, and exposed them to 8 hours/6 hours of OGSD/R with or without edaravone (0...
February 2017: Neural Regeneration Research
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