scholarly journals Insights into Temperature and Hypoxia Tolerance in Cowpea Weevil via HIF-1

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 704
Author(s):  
Qin Liu ◽  
Zhichao Liu ◽  
Zhipeng Gao ◽  
Guanjun Chen ◽  
Changyan Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Survival Rate ◽  
Low Temperature ◽  
Callosobruchus Maculatus ◽  
Human Cancer ◽  
Early Stage ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Tolerance ◽  
Low Oxygen ◽  
Cowpea Weevil

Cowpea weevil (Callosobruchus maculatus) is a major pest that leads to severe damage of the stored leguminous grains. Several management approaches, including physical barriers, biological or chemical methods, are used for controlling bruchid in cowpea. These methods usually target the metabolically active state of weevil. However, it becomes less effective at early stages as egg, larva, or pupa under low temperature and oxygen conditions. Since hypoxia-inducible factor-1 (HIF-1) is known to coordinate multiple gene responses to low oxygen or low temperature signals, we examined the HIF-1α gene expression under low temperature and hypoxic treatments. At −20 °C, it took 4 h to reduce the survival rate for eggs, larvae, and pupae down to 10%, while at 4 °C and 15 °C, the survival rate remained higher than 50% even after 128 h as HIF-1α gene expression peaked at 15 °C. Moreover, HIF-1 protein offers a valuable target for early stage pest control complementary to traditional methods. In particular, HIF-1 inhibitor camptothecin (CPT), one of the five HIF-1 inhibitors examined, achieved a very significant reduction of 96.2% and 95.5% relative to the control in weevil survival rate into adult at 4 °C and 30 °C, respectively. Our study can be used as one model system for drug development in virus infections and human cancer.

Oxygen-dependent gene expression in fishes

2005 ◽  
Vol 288 (5) ◽  
pp. R1079-R1090 ◽  
Author(s):  
Mikko Nikinmaa ◽  
Bernard B. Rees
Keyword(s):  
Gene Expression ◽  
Mammalian Cells ◽  
Hypoxia Inducible Factor ◽  
Transcriptional Response ◽  
Hypoxia Tolerance ◽  
Hypoxic Exposure ◽  
Low Oxygen ◽  
Mammalian Development ◽  
Molecular Responses ◽  
And Function

The role of oxygen in regulating patterns of gene expression in mammalian development, physiology, and pathology has received increasing attention, especially after the discovery of the hypoxia-inducible factor (HIF), a transcription factor that has been likened to a “master switch” in the transcriptional response of mammalian cells and tissues to low oxygen. At present, considerably less is known about the molecular responses of nonmammalian vertebrates and invertebrates to hypoxic exposure. Because many animals live in aquatic habitats that are variable in oxygen tension, it is relevant to study oxygen-dependent gene expression in these animals. The purpose of this review is to discuss hypoxia-induced gene expression in fishes from an evolutionary and ecological context. Recent studies have described homologs of HIF in fish and have begun to evaluate their function. A number of physiological processes are known to be altered by hypoxic exposure of fish, although the evidence linking them to HIF is less well developed. The diversity of fish presents many opportunities to evaluate if inter- and intraspecific variation in HIF structure and function correlate with hypoxia tolerance. Furthermore, as an aquatic group, fish offer the opportunity to examine the interactions between hypoxia and other stressors, including pollutants, common in aquatic environments. It is possible, if not likely, that results obtained by studying the molecular responses of fish to hypoxia will find parallels in the oxygen-dependent responses of mammals, including humans. Moreover, novel responses to hypoxia could be discovered through studies of this diverse and species-rich group.

HIF1-α-Mediated Gene Expression Induced by Vitamin B1 Deficiency

2013 ◽  
Vol 83 (3) ◽  
pp. 188-197 ◽  
Author(s):  
Rebecca L. Sweet ◽  
Jason A. Zastre
Keyword(s):  
Gene Expression ◽  
Thiamine Deficiency ◽  
Glucose Transporter ◽  
Neuroblastoma Cell ◽  
Hypoxia Inducible Factor ◽  
Clinical Manifestations ◽  
Vitamin B1 ◽  
Low Oxygen ◽  
Glucose Transporter 1 ◽  
Metabolic Intermediates

It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.

scholarly journals Hypoxia-Induced Gene Expression Occurs Solely through the Action of Hypoxia-Inducible Factor 1α (HIF-1α): Role of Cytoplasmic Trapping of HIF-2α

2003 ◽  
Vol 23 (14) ◽  
pp. 4959-4971 ◽  
Author(s):  
Sang-ki Park ◽  
Agnes M. Dadak ◽  
Volker H. Haase ◽  
Lucrezia Fontana ◽  
Amato J. Giaccia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Activity ◽  
Hypoxia Inducible Factor ◽  
Low Oxygen ◽  
Hypoxic Conditions ◽  
Show Evidence ◽  
Dependent Protein ◽  
A Cell ◽  
Cell Type Specific ◽  
Inducible Genes

ABSTRACT The hypoxia-inducible factors 1α (HIF-1α) and 2α (HIF-2α) have extensive structural homology and have been identified as key transcription factors responsible for gene expression in response to hypoxia. They play critical roles not only in normal development, but also in tumor progression. Here we report on the differential regulation of protein expression and transcriptional activity of HIF-1α and -2α by hypoxia in immortalized mouse embryo fibroblasts (MEFs). We show that oxygen-dependent protein degradation is restricted to HIF-1α, as HIF-2α protein is detected in MEFs regardless of oxygenation and is localized primarily to the cytoplasm. Endogenous HIF-2α remained transcriptionally inactive under hypoxic conditions; however, ectopically overexpressed HIF-2α translocated into the nucleus and could stimulate expression of hypoxia-inducible genes. We show that the factor inhibiting HIF-1 can selectively inhibit the transcriptional activity of HIF-1α but has no effect on HIF-2α-mediated transcription in MEFs. We propose that HIF-2α is not a redundant transcription factor of HIF-1α for hypoxia-induced gene expression and show evidence that there is a cell type-specific modulator(s) that enables selective activation of HIF-1α but not HIF-2α in response to low-oxygen stress.

Investigating gene expression profile of non-small cell lung cancer

Open Medicine ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. 608-615
Author(s):  
Tõnu Vooder ◽  
Andres Metspalu
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Survival Rate ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Early Stage ◽  
Treatment Strategies ◽  
Small Cell ◽  
Small Cell Lung ◽  
Lung Cancers

AbstractLung cancer is mainly a lifestyle-associated disease with poor prognosis and the lowest five year survival rate of all types of cancer. Lung cancers are divided into two main groups: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). Surgical treatment is generally indicated in cases of early stage NSCLC, and those patients treated with radical and aggressive surgery have a somewhat better survival rate. The main problems with lung cancer treatment are due to late diagnosis, rapidly developing drug resistance and side effects of the treatment that are experienced by almost all patients. The next step for distinguishing histologically complicated lung cancers and determining optimal treatment strategies is gene expression analysis. Supported by gene expression data, it is possible to prognosticate the course of the disease.

scholarly journals Tolerance to Hypoxia Is Promoted by FOXO Regulation of the Innate Immunity Transcription Factor NF-κB/Relish in Drosophila

Genetics ◽  
2020 ◽  
Vol 215 (4) ◽  
pp. 1013-1025 ◽  
Author(s):  
Elizabeth C. Barretto ◽  
Danielle M. Polan ◽  
Amy N. Beevor-Potts ◽  
Byoungchun Lee ◽  
Savraj S. Grewal
Keyword(s):  
Transcription Factor ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Innate Immune ◽  
Hypoxia Tolerance ◽  
Dependent Manner ◽  
Low Oxygen ◽  
Hypoxia Exposure ◽  
Forkhead Box ◽  
Pathological Conditions

Exposure of tissues and organs to low oxygen (hypoxia) occurs in both physiological and pathological conditions in animals. Under these conditions, organisms have to adapt their physiology to ensure proper functioning and survival. Here, we define a role for the transcription factor Forkhead Box-O (FOXO) as a mediator of hypoxia tolerance in Drosophila. We find that upon hypoxia exposure, FOXO transcriptional activity is rapidly induced in both larvae and adults. Moreover, we see that foxo mutant animals show misregulated glucose metabolism in low oxygen and subsequently exhibit reduced hypoxia survival. We identify the innate immune transcription factor, NF-κB/Relish, as a key FOXO target in the control of hypoxia tolerance. We find that expression of Relish and its target genes is increased in a FOXO-dependent manner in hypoxia, and that relish mutant animals show reduced survival in hypoxia. Together, these data indicate that FOXO is a hypoxia-inducible factor that mediates tolerance to low oxygen by inducing immune-like responses.

Persisting mild hypothermia suppresses hypoxia-inducible factor-1α protein synthesis and hypoxia-inducible factor-1-mediated gene expression

2010 ◽  
Vol 298 (3) ◽  
pp. R661-R671 ◽  
Author(s):  
Tomoharu Tanaka ◽  
Takuhiko Wakamatsu ◽  
Hiroki Daijo ◽  
Seiko Oda ◽  
Shinichi Kai ◽  
...  
Keyword(s):  
Gene Expression ◽  
Low Temperature ◽  
Hypoxia Inducible Factor ◽  
The Body ◽  
The Other ◽  
Adaptation To Hypoxia ◽  
Hypoxia Inducible Factor 1 ◽  
Other Hand

The transcription factor hypoxia-inducible factor-1 (HIF-1) plays an essential role in regulating gene expression in response to hypoxia-ischemia. Ischemia causes the tissue not only to be hypoxic but also to be hypothermic because of the hypoperfusion under certain circumstances. On the other hand, the induced hypothermia is one of the most common therapeutic modalities to extend tolerance to hypoxia. Although hypoxia elicits a variety of cellular and systemic responses at different organizational levels in the body, little is known about how hypoxia-induced responses are affected by low temperature. We examined the influence of mild hypothermic conditions (28–32°C) on HIF-1 in both in vitro and in vivo settings. In vitro experiments adopting cultured cells elucidated that hypoxia-induced HIF-1 activation was resistant to 4-h exposure to the low temperature. In contrast, exposure to the low temperature as long as 24 h suppressed HIF-1 activation and the subsequent upregulation of HIF-1 target genes such as VEGF or GLUT-1. HIF-1α protein stability in the cell was not affected by hypothermic treatment. Furthermore, intracellular ATP content was reduced under 1% O2 conditions but was not largely affected by hypothermic treatment. The evidence indicates that reduction of oxygen consumption is not largely involved in suppression of HIF-1. In addition, we demonstrated that HIF-1 DNA-binding activity and HIF-1-dependent gene expressions induced under 10% O2 atmosphere in mouse brain were not influenced by treatment under 3-h hypothermic temperature but were inhibited under 5-h treatment. On the other hand, we indicated that warming ischemic legs of mice for 24 h preserved HIF-1 activity. In this report we describe for the first time that persisting low temperature significantly reduced HIF-1α neosynthesis under hypoxic conditions, leading to a decrease in gene expression for adaptation to hypoxia in both in vitro and in vivo settings.

scholarly journals Transcriptome sequencing revealed differences in the response of renal cancer cells to hypoxia and CoCl2 treatment

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 1518 ◽  
Author(s):  
Nadezhda Zhigalova ◽  
Artem Artemov ◽  
Alexander M. Mazur ◽  
Egor B. Prokhortchouk
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Hypoxia Inducible Factor ◽  
Low Oxygen ◽  
Human Cancer Cells ◽  
Hypoxic Conditions ◽  
Pathway Activation ◽  
Oxygen Conditions ◽  
Order Of Magnitude ◽  
Transcriptional Changes

Human cancer cells are subjected to hypoxic conditions in many tumours. Hypoxia causes alterations in the glycolytic pathway activation through stabilization of hypoxia-inducible factor 1. Currently, two approaches are commonly used to model hypoxia: an alternative to generating low-oxygen conditions in an incubator, cells can be treated with CoCl2. We performed RNA-seq experiments to study transcriptomes of human Caki-1 cells under real hypoxia and after CoCl2 treatment. Despite causing transcriptional changes of a much higher order of magnitude for the genes in the hypoxia regulation pathway, CoCl2 treatment fails to induce alterations in the glycolysis / gluconeogenesis pathway. Moreover, CoCl2 caused aberrant activation of other oxidoreductases in glycine, serine and threonine metabolism pathways.

scholarly journals Glutamine Homeostasis and Its Role in the Adaptive Strategies of the Blind Mole Rat, Spalax

Metabolites ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 755
Author(s):  
Dmitry Miskevich ◽  
Anastasia Chaban ◽  
Maria Dronina ◽  
Ifat Abramovich ◽  
Eyal Gottlieb ◽  
...  
Keyword(s):  
Healthy Aging ◽  
Pyruvate Dehydrogenase Complex ◽  
Hypoxia Inducible Factor ◽  
Primary Source ◽  
Hypoxia Tolerance ◽  
Cancer Resistance ◽  
Low Oxygen ◽  
Hypoxic Conditions ◽  
Mole Rat ◽  
Tightly Coupled

Oxidative metabolism is fine-tuned machinery that combines two tightly coupled fluxes of glucose and glutamine-derived carbons. Hypoxia interrupts the coordination between the metabolism of these two nutrients and leads to a decrease of the system efficacy and may eventually cause cell death. The subterranean blind mole rat, Spalax, is an underexplored, underground, hypoxia-tolerant mammalian group which spends its life under sharply fluctuating oxygen levels. Primary Spalax cells are an exceptional model to study the metabolic strategies that have evolved in mammals inhabiting low-oxygen niches. In this study we explored the metabolic frame of glutamine (Gln) homeostasis in Spalax skin cells under normoxic and hypoxic conditions and their impacts on the metabolism of rat cells. Targeted metabolomics employing liquid chromatography and mass spectrometry (LC-MS) was used to track the fate of heavy glutamine carbons (13C5 Gln) after 24 h under normoxia or hypoxia (1% O2). Our results indicated that large amounts of glutamine-originated carbons were detected as proline (Pro) and hydroxyproline (HPro) in normoxic Spalax cells with a further increase under hypoxia, suggesting a strategy for reduced Gln carbons storage in proteins. The intensity of the flux and the presence of HPro suggests collagen as a candidate protein that is most abundant in animals, and as the primary source of HPro. An increased conversion of αKG to 2 HG that was indicated in hypoxic Spalax cells prevents the degradation of hypoxia-inducible factor 1α (HIF-1α) and, consequently, maintains cytosolic and mitochondrial carbons fluxes that were uncoupled via inhibition of the pyruvate dehydrogenase complex. A strong antioxidant defense in Spalax cells can be attributed, at least in part, to the massive usage of glutamine-derived glutamate for glutathione (GSH) production. The present study uncovers additional strategies that have evolved in this unique mammal to support its hypoxia tolerance, and probably contribute to its cancer resistance, longevity, and healthy aging.

scholarly journals Hypoxia-Inducible Factor 2 Regulates Hepatic Lipid Metabolism

2009 ◽  
Vol 29 (16) ◽  
pp. 4527-4538 ◽  
Author(s):  
Erinn B. Rankin ◽  
Jennifer Rha ◽  
Mary A. Selak ◽  
Travis L. Unger ◽  
Brian Keith ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Hypoxia Inducible Factor ◽  
Hepatic Tissue ◽  
Low Oxygen ◽  
Hepatic Lipid Metabolism ◽  
Peripheral Tissues ◽  
Hepatic Lipid ◽  
Normal Hepatocyte ◽  
Oxygen Sensitive

ABSTRACT In mammals, the liver integrates nutrient uptake and delivery of carbohydrates and lipids to peripheral tissues to control overall energy balance. Hepatocytes maintain metabolic homeostasis by coordinating gene expression programs in response to dietary and systemic signals. Hepatic tissue oxygenation is an important systemic signal that contributes to normal hepatocyte function as well as disease. Hypoxia-inducible factors 1 and 2 (HIF-1 and HIF-2, respectively) are oxygen-sensitive heterodimeric transcription factors, which act as key mediators of cellular adaptation to low oxygen. Previously, we have shown that HIF-2 plays an important role in both physiologic and pathophysiologic processes in the liver. HIF-2 is essential for normal fetal EPO production and erythropoiesis, while constitutive HIF-2 activity in the adult results in polycythemia and vascular tumorigenesis. Here we report a novel role for HIF-2 in regulating hepatic lipid metabolism. We found that constitutive activation of HIF-2 in the adult results in the development of severe hepatic steatosis associated with impaired fatty acid β-oxidation, decreased lipogenic gene expression, and increased lipid storage capacity. These findings demonstrate that HIF-2 functions as an important regulator of hepatic lipid metabolism and identify HIF-2 as a potential target for the treatment of fatty liver disease.

scholarly journals FOXO mediates organismal hypoxia tolerance by regulating NF-κB in Drosophila

2019 ◽  
Author(s):  
Elizabeth C Barretto ◽  
Danielle M Polan ◽  
Amy N Beever-Potts ◽  
Byoungchun Lee ◽  
Savraj S Grewal
Keyword(s):  
Transcription Factor ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Innate Immune ◽  
Hypoxia Tolerance ◽  
Dependent Manner ◽  
Low Oxygen ◽  
Hypoxia Exposure ◽  
Pathological Conditions ◽  
Nf Kappab

ABSTRACTExposure of tissues and organs to low oxygen (hypoxia) occurs in both physiological and pathological conditions in animals. Under these conditions, organisms have to adapt their physiology to ensure proper functioning and survival. Here we define a role for the transcription factor FOXO as a mediator of hypoxia tolerance in Drosophila. We find that upon hypoxia exposure, FOXO transcriptional activity is rapidly induced in both larvae and adults. Moreover, we see that foxo mutant animals show misregulated glucose metabolism in low oxygen and subsequently exhibit reduced hypoxia survival. We identify the innate immune transcription factor, NF-KappaB/Relish, as a key FOXO target in the control of hypoxia tolerance. We find that expression of Relish and its target genes are increase in a FOXO-dependent manner in hypoxia, and that relish mutant animals show reduced survival in hypoxia. Together, these data indicate that FOXO is a hypoxia inducible factor that mediates tolerance to low oxygen by inducing immune-like responses.

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