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Comparative Biochemistry and... May 2022In anoxia-sensitive mammals, hypoxia inducible factor (HIF) promotes cellular survival in hypoxia, but also tumorigenesis. By comparison, anoxia-tolerant vertebrates...
Gene expression of hypoxia-inducible factor (HIF), HIF regulators, and putative HIF targets in ventricle and telencephalon of Trachemys scripta acclimated to 21 °C or 5 °C and exposed to normoxia, anoxia or reoxygenation.
In anoxia-sensitive mammals, hypoxia inducible factor (HIF) promotes cellular survival in hypoxia, but also tumorigenesis. By comparison, anoxia-tolerant vertebrates likely need to circumvent a prolonged upregulation of HIF to survive long-term anoxia, making them attractive biomedical models for investigating HIF regulation. To lend insight into the role of HIF in anoxic Trachemys scripta ventricle and telencephalon, 21 °C- and 5 °C-acclimated turtles were exposed to normoxia, anoxia (24 h at 21 °C; 24 h or 14 d at 5 °C) or anoxia + reoxygenation and the gene expression of HIF-1α (hif1a) and HIF-2α (hif2a), two regulators of HIF, and eleven putative downstream targets of HIF quantified by qPCR. Changes in gene expression with anoxia at 21 °C differentially aligned with a circumvention of HIF activity. Whereas hif1a and hif2a expression was unaffected in ventricle and telencephalon, and BCL2 interacting protein 3 gene expression reduced by 30% in telencephalon, gene expression of vascular endothelial growth factor-A increased in ventricle (4.5-fold) and telencephalon (1.5-fold), and hexokinase 1 (2-fold) and hexokinase 2 (3-fold) gene expression increased in ventricle. At 5 °C, the pattern of gene expression in ventricle or telencephalon was unaltered with oxygenation state. However, cold acclimation in normoxia induced downregulation of HIF-1α, HIF-2α, and HIF target gene expression in telencephalon. Overall, the findings lend support to the postulation that prolonged activation of HIF is counterproductive for long-term anoxia survival. Nevertheless, quantification of the effect of anoxia and acclimation temperature on HIF binding activity and regulation at the protein level are needed to provide a strong scientific framework whereby new strategies for oxygen related pathologies can be developed.
Topics: Acclimatization; Animals; Gene Expression; Hypoxia; Mammals; Telencephalon; Turtles; Vascular Endothelial Growth Factor A
PubMed: 35182763
DOI: 10.1016/j.cbpa.2022.111167 -
Annals of the New York Academy of... Feb 2016Surviving hypoxia is one of the most critical challenges faced by vertebrates. Most species have adapted to changing levels of oxygen in their environment with... (Review)
Review
Surviving hypoxia is one of the most critical challenges faced by vertebrates. Most species have adapted to changing levels of oxygen in their environment with specialized organs that sense hypoxia, while only few have been uniquely adapted to survive prolonged periods of anoxia. The goal of this review is to present the most recent research on oxygen sensing, adaptation to hypoxia, and mechanisms of anoxia tolerance in nonmammalian vertebrates. We discuss the respiratory structures in fish, including the skin, gills, and air-breathing organs, and recent evidence for chemosensory neuroepithelial cells (NECs) in these tissues that initiate reflex responses to hypoxia. The use of the zebrafish as a genetic and developmental model has allowed observation of the ontogenesis of respiratory and chemosensory systems, demonstration of a putative intracellular O2 sensor in chemoreceptors that may initiate transduction of the hypoxia signal, and investigation into the effects of extreme hypoxia on cardiorespiratory development. Other organisms, such as goldfish and freshwater turtles, display a high degree of anoxia tolerance, and these models are revealing important adaptations at the cellular level, such as the regulation of glutamatergic and GABAergic neurotransmission in defense of homeostasis in central neurons.
Topics: Adaptation, Physiological; Animals; Chemoreceptor Cells; Gills; Homeostasis; Humans; Hypoxia; Skin; Zebrafish
PubMed: 25959851
DOI: 10.1111/nyas.12780 -
Journal of Visualized Experiments : JoVE Mar 2014Protocols for anoxia/starvation in the genetic model organism C. elegans simulate ischemia/reperfusion. Worms are separated from bacterial food and placed under anoxia...
Protocols for anoxia/starvation in the genetic model organism C. elegans simulate ischemia/reperfusion. Worms are separated from bacterial food and placed under anoxia for 20 hr (simulated ischemia), and subsequently moved to a normal atmosphere with food (simulated reperfusion). This experimental paradigm results in increased death and neuronal damage, and techniques are presented to assess organism viability, alterations to the morphology of touch neuron processes, as well as touch sensitivity, which represents the behavioral output of neuronal function. Finally, a method for constructing hypoxic incubators using common kitchen storage containers is described. The addition of a mass flow control unit allows for alterations to be made to the gas mixture in the custom incubators, and a circulating water bath allows for both temperature control and makes it easy to identify leaks. This method provides a low cost alternative to commercially available units.
Topics: Animals; Behavior, Animal; Caenorhabditis elegans; Disease Models, Animal; Hypoxia; Ischemia; Neurons; Reperfusion; Starvation
PubMed: 24637332
DOI: 10.3791/51231 -
Biomolecules Oct 2021The red-eared slider () undergoes numerous changes to its physiological and metabolic processes to survive without oxygen. During anoxic conditions, its metabolic rate...
The red-eared slider () undergoes numerous changes to its physiological and metabolic processes to survive without oxygen. During anoxic conditions, its metabolic rate drops drastically to minimize energy requirements. The alterations in the central metabolic pathways are often accomplished by the regulation of key enzymes. The regulation of one such enzyme, fructose-1,6-bisphosphatase (FBPase; EC 3.1.3.11), was characterized in the present study during anoxia in liver. FBPase is a crucial enzyme of gluconeogenesis. The FBPase was purified from liver tissue in both control and anoxic conditions and subsequently assayed to determine the kinetic parameters of the enzyme. The study revealed the relative degree of post-translational modifications in the FBPase from control and anoxic turtles. Further, this study demonstrated a significant decrease in the maximal activity in anoxic FBPase and decreased sensitivity to its substrate Fructose-1,6-bisphosphate (FBP) when compared to the control. Immunoblotting demonstrated increased threonine phosphorylation (~1.4-fold) in the anoxic FBPase. Taken together, these results suggest that the phosphorylation of liver FBPase is an important step in suppressing FBPase activity, ultimately leading to the inhibition of gluconeogenesis in the liver of the red-eared slider during anaerobic conditions.
Topics: Animals; Fructose; Fructose-Bisphosphatase; Hypoxia; Liver; Oxygen; Phosphorylation; Protein Processing, Post-Translational; Signal Transduction; Turtles
PubMed: 34680181
DOI: 10.3390/biom11101548 -
Archives of Internal Medicine Jul 1962
Topics: Humans; Hypoxia; Hypoxia, Brain
PubMed: 14487254
DOI: 10.1001/archinte.1962.03620190020003 -
JAMA Mar 1963
Topics: Animals; Brain; Dogs; Humans; Hypoxia; Hypoxia, Brain
PubMed: 13937894
DOI: 10.1001/jama.1963.63700130004011a -
Proceedings of the Royal Society of... Sep 1956
Topics: Anesthesia; Hypoxia; Iatrogenic Disease; Nervous System Diseases
PubMed: 13379359
DOI: No ID Found -
Neuroscience Letters Oct 2019Asphyxia before, during, or after birth is an important cause of perinatal mortality and morbidity. The mechanism underlying neurological damage resulting from anoxia...
Asphyxia before, during, or after birth is an important cause of perinatal mortality and morbidity. The mechanism underlying neurological damage resulting from anoxia episode is complex and is not limited to the anoxia episode. Although the benefits of therapeutic hypothermia in secondary failure of oxidative metabolism have long been known, the principle of this therapy in tertiary phase of repair and reorganization have not yet to be fully elucidated. Currently brain-derived neurotrophic factor (BDNF) is also considered to be beneficial to neuronal survival. Therefore, our experiments aimed at determining the effects of low body temperature during simulated perinatal anoxia on the level of the neurotrophic brain-derived factor (BDNF) and on the correlation between the level of BDNF (proBDNF and mBDNF) and the level of active caspase-3 (marker of apoptosis) in developing brain in tertiary phase after exposure. The results demonstrated that the ability of BDNF to inhibit caspase-3 activation and subsequent apoptosis likely accounts in large part for its protection against neuronal damage only in rats maintaining the low body temperature.
Topics: Animals; Animals, Newborn; Apoptosis; Brain; Brain-Derived Neurotrophic Factor; Caspase 3; Female; Hypothermia, Induced; Hypoxia; Male; Rats; Rats, Wistar
PubMed: 31394123
DOI: 10.1016/j.neulet.2019.134413 -
Lancet (London, England) Jul 1957
Topics: Emphysema; Humans; Hypoxia; Oxygen; Pulmonary Emphysema; Social Behavior
PubMed: 13450349
DOI: No ID Found -
Brain Research Aug 1993Cerebral ischemia induces major neuronal morphological alterations. It is not clear, however, whether this is directly caused by O2 deprivation. To determine the effect...
Cerebral ischemia induces major neuronal morphological alterations. It is not clear, however, whether this is directly caused by O2 deprivation. To determine the effect of hypoxia on cytoskeletal structures and neuronal morphology, we performed experiments and examined anoxia-induced changes in microtubule-associated protein 2 (MAP2) and cell morphology in hippocampal slices in vitro. Anoxia (measured PO2 = 0 Torr) induced a marked loss in dendritic MAP2 immunoreactivity and cell swelling of hippocampal neurons by 2 h after O2 reinstitution. These changes were severe in CA1 and CA3 neurons and comparatively mild in dentate gyrus neurons. Quantitative analysis showed that 10 min of anoxia induced a 30% loss of MAP2-positive dendrites but this increased to 70% after 30 min of anoxia. A concurrent major increase in somata area of about 100% and 200% was observed in CA1 and CA3 neurons respectively. Somata area in the lower dentate gyrus, however, increased either insignificantly or by only 30% for the respective periods of anoxia. These results suggest that deprivation of O2 can by itself induce a major loss in dendritic MAP2 immunoreactivity and changes in cell morphology in hippocampal neurons. These alterations occur rapidly after hypoxia, and the severity of these changes is directly related to the duration of anoxia and brain region in the hippocampus.
Topics: Animals; Hippocampus; Hypoxia; In Vitro Techniques; Kinetics; Microtubule-Associated Proteins; Neurons; Rats; Rats, Sprague-Dawley; Time Factors
PubMed: 8369956
DOI: 10.1016/0006-8993(93)90157-i