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Glucose deprivation

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https://www.readbyqxmd.com/read/28107516/liver-amp-activated-protein-kinase-is-unnecessary-for-gluconeogenesis-but-protects-energy-state-during-nutrient-deprivation
#1
Clinton M Hasenour, D Emerson Ridley, Freyja D James, Curtis C Hughey, E Patrick Donahue, Benoit Viollet, Marc Foretz, Jamey D Young, David H Wasserman
AMPK is an energy sensor that protects cellular energy state by attenuating anabolic and promoting catabolic processes. AMPK signaling is purported to regulate hepatic gluconeogenesis and substrate oxidation; coordination of these processes is vital during nutrient deprivation or pathogenic during overnutrition. Here we directly test hepatic AMPK function in regulating metabolic fluxes that converge to produce glucose and energy in vivo. Flux analysis was applied in mice with a liver-specific deletion of AMPK (L-KO) or floxed control littermates to assess rates of hepatic glucose producing and citric acid cycle (CAC) fluxes...
2017: PloS One
https://www.readbyqxmd.com/read/28106780/integrins-and-cell-metabolism-an-intimate-relationship-impacting-cancer
#2
REVIEW
Rehman Ata, Costin N Antonescu
Integrins are important regulators of cell survival, proliferation, adhesion and migration. Once activated, integrins establish a regulated link between the extracellular matrix and the cytoskeleton. Integrins have well-established functions in cancer, such as in controlling cell survival by engagement of many specific intracellular signaling pathways and in facilitating metastasis. Integrins and associated proteins are regulated by control of transcription, membrane traffic, and degradation, as well as by a number of post-translational modifications including glycosylation, allowing integrin function to be modulated to conform to various cellular needs and environmental conditions...
January 18, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28106772/neuroprotective-and-anti-apoptotic-effects-of-csp-1103-in-primary-cortical-neurons-exposed-to-oxygen-and-glucose-deprivation
#3
Vanessa Porrini, Ilenia Sarnico, Marina Benarese, Caterina Branca, Mariana Mota, Annamaria Lanzillotta, Arianna Bellucci, Edoardo Parrella, Lara Faggi, Pierfranco Spano, Bruno Pietro Imbimbo, Marina Pizzi
CSP-1103 (formerly CHF5074) has been shown to reverse memory impairment and reduce amyloid plaque as well as inflammatory microglia activation in preclinical models of Alzheimer's disease. Moreover, it was found to improve cognition and reduce brain inflammation in patients with mild cognitive impairment. Recent evidence suggests that CSP-1103 acts through a single molecular target, the amyloid precursor protein intracellular domain (AICD), a transcriptional regulator implicated in inflammation and apoptosis...
January 18, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28105979/human-dental-pulp-stem-cells-are-more-effective-than-human-bone-marrow-derived-mesenchymal-stem-cells-in-cerebral-ischemic-injury
#4
Miyeoun Song, Jae-Hyung Lee, Jinhyun Bae, Youngmin Bu, Eun-Cheol Kim
We compared the therapeutic effects and mechanism of transplanted human dental pulp stem cells (hDPSCs) and human bonemarrow-derived mesenchymal stem cells (hMSCs) in a stroke model of rats and an <i>in vitro</i> ischemic model. Both hDPSCs- and hMSCs- intravenously injected rats 24&#8201;h after middle cerebral artery occlusion showed improved functional recovery and reduced infarct volume versus control rats, but the hDPSCs group showed greater reduction in infarct volume than hMSCs. The positive area for the endothelial cell marker was greater in the lesion boundary areas in the hDPSCs group than with hMSCs...
January 20, 2017: Cell Transplantation
https://www.readbyqxmd.com/read/28103118/park2-dependent-mitophagy-induced-by-acidic-postconditioning-protects-against-focal-cerebral-ischemia-and-extends-the-reperfusion-window
#5
Zhe Shen, Yanrong Zheng, Jiaying Wu, Ying Chen, Xiaoli Wu, Yiting Zhou, Yang Yuan, Shousheng Lu, Lei Jiang, Zhenghong Qin, Zhong Chen, Weiwei Hu, Xiangnan Zhang
Prompt reperfusion after cerebral ischemia is critical for neuronal survival. Any strategies that extend the limited reperfusion window will be of great importance. Acidic postconditioning (APC) is a mild acidosis treatment that involves inhaling CO2 during reperfusion following ischemia. APC attenuates ischemic brain injury although the underlying mechanisms have not been elucidated. Here we report that APC reinforces ischemia-reperfusion-induced mitophagy in middle cortical artery occlusion (MCAO)-treated mice, and in oxygen-glucose deprivation (OGD)-treated brain slices and neurons...
January 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28101763/mir-126-affects-brain-heart-interaction-after-cerebral-ischemic-stroke
#6
Jieli Chen, Chengcheng Cui, Xiaoping Yang, Jiang Xu, Poornima Venkat, Alex Zacharek, Peng Yu, Michael Chopp
Cardiovascular diseases are approximately three times higher in patients with neurological deficits than in patients without neurological deficits. MicroRNA-126 (MiR-126) facilitates vascular remodeling and decreases fibrosis and is emerging as an important factor in the pathogenesis of cardiovascular diseases and cerebral stroke. In this study, we tested the hypothesis that decreased miR-126 after ischemic stroke may play an important role in regulating cardiac function. Wild-type (WT), specific conditional-knockout endothelial cell miR-126 (miR-126(EC-/-)), and miR-126 knockout control (miR-126(fl/fl)) mice were subjected to distal middle cerebral artery occlusion (dMCAo) (n = 10/group)...
January 19, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28100752/differential-vulnerability-of-ca1-versus-ca3-pyramidal-neurons-after-ischemia-possible-relationship-to-sources-of-zn2-accumulation-and-its-entry-into-and-prolonged-effects-on-mitochondria
#7
Yuliya V Medvedeva, Sung G Ji, Hong Z Yin, John H Weiss
: Excitotoxic mechanisms contribute to the degeneration of hippocampal pyramidal neurons after recurrent seizures and brain ischemia. However, susceptibility differs, with CA1 neurons degenerating preferentially after global ischemia and CA3 neurons after limbic seizures. Whereas most studies address contributions of excitotoxic Ca(2+) entry, it is apparent that Zn(2+) also contributes, reflecting accumulation in neurons either after synaptic release and entry through postsynaptic channels or upon mobilization from intracellular Zn(2+)-binding proteins such as metallothionein-III (MT-III)...
January 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28093214/the-upr-reduces-glucose-metabolism-via-ire1-signaling
#8
Judith M van der Harg, Jessica C van Heest, Fabian N Bangel, Sanne Patiwael, Jan R T van Weering, Wiep Scheper
Neurons are highly dependent on glucose. A disturbance in glucose homeostasis therefore poses a severe risk that is counteracted by activation of stress responses to limit damage and restore the energy balance. A major stress response that is activated under conditions of glucose deprivation is the unfolded protein response (UPR) that is aimed to restore proteostasis in the endoplasmic reticulum. The key signaling of the UPR involves the transient activation of a transcriptional program and an overall reduction of protein synthesis...
January 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28092083/role-of-dopamine-d2-d3-receptors-in-development-plasticity-and-neuroprotection-in-human-ipsc-derived-midbrain-dopaminergic-neurons
#9
Federica Bono, Paola Savoia, Adele Guglielmi, Massimo Gennarelli, Giovanna Piovani, Sandra Sigala, Damiana Leo, Stefano Espinoza, Raul R Gainetdinov, Paola Devoto, PierFranco Spano, Cristina Missale, Chiara Fiorentini
The role of dopamine D2 and D3 receptors (D2R/D3R), located on midbrain dopaminergic (DA) neurons, in the regulation of DA synthesis and release and in DA neuron homeostasis has been extensively investigated in rodent animal models. By contrast, the properties of D2R/D3R in human DA neurons have not been elucidated yet. On this line, the use of human-induced pluripotent stem cells (hiPSCs) for producing any types of cells has offered the innovative opportunity for investigating the human neuronal phenotypes at the molecular levels...
January 14, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28087461/low-glucose-stress-decreases-cellular-nadh-and-mitochondrial-atp-in-colonic-epithelial-cancer-cells-influence-of-mitochondrial-substrates
#10
Magdalena L Circu, Ronald E Maloney, Tak Yee Aw
In this study, we investigated how colonic epithelial cells maintained pyridine nucleotide (NADH/NAD(+)) redox homeostasis upon acute metabolic variation imposed by glucose deprivation or supplementation with mitochondrial substrates, succinate and malate/glutamate (M/G). Our results showed that low glucose caused cellular NADH/NAD(+) redox imbalance that diminished lactate dehydrogenase (LDH) activity and resulted in lower lactate contents. The concurrent activation of malic enzyme (ME) suggested a role for malate in preserving cellular pyruvate that remained unchanged at low glucose...
January 10, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28072729/hypertonic-saline-protects-brain-endothelial-cells-against-hypoxia-correlated-to-the-levels-of-estimated-glomerular-filtration-rate-and-interleukin-1%C3%AE
#11
Sheng-Long Chen, Yi-Yu Deng, Qiao-Sheng Wang, Yong-Li Han, Wen-Qiang Jiang, Ming Fang, Bei Hu, Zhi-Xin Wu, Lin-Qiang Huang, Hong-Ke Zeng
OBJECTIVE: The aim of this study was to verify the protective effect of hypertonic saline (HS) on brain endothelial cells under hypoxic conditions and the relevant underlying mechanism. METHODS: bEnd.3 cells were treated with oxygen-glucose deprivation (OGD)-induced injury. To measure HS performance, cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt assay, and cell apoptosis was assessed by flow cytometry and Terminal deoxynucleotidyl transferase UTP nick-end labeling staining...
January 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28069924/soluble-cpg15-from-astrocytes-ameliorates-neurites-outgrowth-recovery-of-hippocampal-neurons-after-mouse-cerebral-ischemia
#12
Jing-Jing Zhao, Jie-Xian Hu, De-Xin Lu, Chun-Xia Ji, Yao Qi, Xiao-Yan Liu, Feng-Yan Sun, Fang Huang, Ping Xu, Xian-Hua Chen
The present study focuses on the function of cpg15, a neurotrophic factor, in ischemic neuronal recovery using transient global cerebral ischemic (TGI) mouse model and oxygen-glucose deprivation (OGD)-treated primary cultured cells. The results showed that expression of cpg15 proteins in astrocytes, predominantly the soluble form, was significantly increased in mouse hippocampus after TGI and in the cultured astrocytes after OGD. Addition of the medium from the cpg15-overexpressed astrocytic culture into the OGD-treated hippocampal neuronal cultures reduces the neuronal injury, while the recovery of neurite outgrowths of OGD-injured neurons was prevented when cpg15 in the OGD-treated astrocytes was knocked down, or the OGD treated-astrocytic medium was immunoabsorbed by cpg15 antibody...
January 9, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28069826/endostatin-inhibits-androgen-independent-prostate-cancer-growth-by-suppressing-nuclear-receptor-mediated-oxidative-stress
#13
Joo Hyoung Lee, Minsung Kang, Hong Wang, Gurudatta Naik, James A Mobley, Guru Sonpavde, W Timothy Garvey, Victor M Darley-Usmar, Selvarangan Ponnazhagan
Androgen-deprivation therapy has been identified to induce oxidative stress in prostate cancer (PCa), leading to reactivation of androgen receptor (AR) signaling in a hormone-refractory manner. Thus, antioxidant therapies have gained attention as adjuvants for castration-resistant PCa. Here, we report for the first time that human endostatin (ES) prevents androgen-independent growth phenotype in PCa cells through its molecular targeting of AR and glucocorticoid receptor (GR) and downstream pro-oxidant signaling...
January 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28069379/ndrg2-overexpression-suppresses-hepatoma-cells-survival-during-metabolic-stress-through-disturbing-the-activation-of-fatty-acid-oxidation
#14
Tao Pan, Mei Zhang, Fang Zhang, Guang Yan, Yi Ru, Qinhao Wang, Yao Zhang, Xuehui Wei, Xinyuan Xu, Lan Shen, Jian Zhang, Kaichun Wu, Libo Yao, Xia Li
Because of the high nutrient consumption and inadequate vascularization, solid tumor constantly undergoes metabolic stress during tumor development. Oncogenes and tumor suppressor genes participated in cancer cells' metabolic reprogramming. N-Myc downstream regulated gene 2 (NDRG2) is a recently identified tumor suppressor gene, but its function in cancer metabolism, particularly during metabolic stress, remains unclear. In this study, we found that NDRG2 overexpression significantly reduced hepatoma cell proliferation and enhanced cell apoptosis under glucose limitation...
January 6, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28065687/restless-legs-syndrome-and-cardiovascular-disease-a-research-roadmap
#15
REVIEW
Daniel J Gottlieb, Virend K Somers, Naresh M Punjabi, John W Winkelman
In this paper, we first critically appraise the epidemiologic literature examining the association of restless legs syndrome (RLS) with cardiovascular disease (CVD) and then consider whether lessons learned from the study of cardiovascular consequences of other sleep disorders might inform a research agenda to examine the potential mechanisms of cardiovascular morbidity of RLS. Cross-sectional and longitudinal studies are both mixed as to whether there is a meaningful association of RLS and CVD. On the other hand, numerous cross-sectional and longitudinal observational studies have shown a strong association of obstructive sleep apnea (OSA) with CVD risk...
October 27, 2016: Sleep Medicine
https://www.readbyqxmd.com/read/28057538/neuropeptide-y-y2-and-y5-receptors-as-promising-targets-for-neuroprotection-in-primary-neurons-exposed-to-oxygen-glucose-deprivation-and-in-transient-focal-cerebral-ischemia-in-rats
#16
Helena Domin, Łukasz Przykaza, Danuta Jantas, Ewa Kozniewska, Paweł M Boguszewski, Maria Śmiałowska
It was postulated that neuropeptide Y (NPY)-ergic system could be involved in the ischemic pathophysiology, however, the role of particular subtypes of NPY receptors (YRs) in neuroprotection against ischemia is still not well known. Therefore, we investigated the effect of NPY and YR ligands using in vitro and in vivo experimental ischemic stroke models. Our in vitro findings showed that NPY (0.5-1μM) and specific agonists of Y2R (0.1-1μM) and Y5R (0.5-1μM) but not that of Y1R produced neuroprotective effects against oxygen-glucose deprivation (OGD)-induced neuronal cell death, being also effective when given 30min after the end of OGD...
January 3, 2017: Neuroscience
https://www.readbyqxmd.com/read/28056323/-the-role-of-neuroglobin-in-oxygen-glucose-deprivation-and-reoxygenation-induced-mitochondrial-depolarization-and-reactive-oxygen-species-production-in-sh-sy5y-cells
#17
S Y Deng, Y H Ai, L N Zhang, L Wu, C X Chen, Y M Wang, Z Y Liu, L Huang, Q Y Peng
Objective: To investigate the role of neuroglobin (NGB) in oxygen-glucose deprivation and reoxygenation (OGD/R) induced mitochondrial depolarization and reactive oxygen species (ROS)production in a human neuroblastoma cell line (SH-SY5Y). Methods: SH-SY5Y cells were transfected with lentivirus to establish a stable cell line of NGB knockdown (KD). After treated with OGD/R, cells were collected at different time points to analyze NGB mRNA and protein levels. Furthermore, cells were stained with JC-1 and DCFH-DA to evaluate mitochondrial depolarization and ROS production by inverted fluorescence microscope...
January 1, 2017: Zhonghua Nei Ke za Zhi [Chinese Journal of Internal Medicine]
https://www.readbyqxmd.com/read/28054002/data-on-pharmacological-applications-and-hypothermia-protection-against-in-vitro-oxygen-glucose-deprivation-related-neurodegeneration-of-adult-rat-ca1-region
#18
Pınar Öz, Hale Saybaşılı
In this data article, the level of chemical neuroprotection against oxygen-glucose-deprivation (OGD)-related neurodegeneration in CA1 was analyzed using the measurements on CA1 stratum pyramidale (CA1sp) width. Adult rat hippocampal slices were incubated in OGD medium for 60 min to create a model for severe ischemic conditions. Alternatively, control slices were incubated in artificial cerebrospinal fluid (ACSF) for 60 min. A study of OGD induced neurodegeneration and partial prevention by pharmacological agents reported; baclofen, memantine and l-carnitine effects were included...
February 2017: Data in Brief
https://www.readbyqxmd.com/read/28039150/the-effects-and-regulatory-mechanism-of-rip3-on-rgc-5-necroptosis-following-elevated-hydrostatic-pressure
#19
Lei Shang, Wei Ding, Na Li, Lvshuang Liao, Dan Chen, Jufang Huang, Kun Xiong
Necroptosis is a type of regulated cell death that has been implicated in various diseases. Receptor-interacting protein 3 (RIP3), a member of the RIP family, is an important mediator of the necroptotic pathway. Cleavage of RIP3 at Asp328 by caspase-8 abolishes the kinase activity of RIP3, which is critical for necroptosis. Moreover, RIP3 is significantly upregulated during the early stages of acute high intra-ocular pressure and oxygen glucose deprivation. In this study, the effects of RIP3 during elevated hydrostatic pressure (EHP) were investigated and the possible mechanism through which caspase-8 regulated RIP3 cleavage was explored...
December 29, 2016: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/28032919/expression-of-the-human-isoform-of-glutamate-dehydrogenase-hgdh2-augments-tca-cycle-capacity-and-oxidative-metabolism-of-glutamate-during-glucose-deprivation-in-astrocytes
#20
Jakob D Nissen, Kasper Lykke, Jaroslaw Bryk, Malin H Stridh, Ioannis Zaganas, Dorte M Skytt, Arne Schousboe, Lasse K Bak, Wolfgang Enard, Svante Pääbo, Helle S Waagepetersen
A key enzyme in brain glutamate homeostasis is glutamate dehydrogenase (GDH) which links carbohydrate and amino acid metabolism mediating glutamate degradation to CO2 and expanding tricarboxylic acid (TCA) cycle capacity with intermediates, i.e. anaplerosis. Humans express two GDH isoforms, GDH1 and 2, whereas most other mammals express only GDH1. hGDH1 is widely expressed in human brain while hGDH2 is confined to astrocytes. The two isoforms display different enzymatic properties and the nature of these supports that hGDH2 expression in astrocytes potentially increases glutamate oxidation and supports the TCA cycle during energy-demanding processes such as high intensity glutamatergic signaling...
December 29, 2016: Glia
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