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Relevant bibliographies by topics / Hypoxia regulators

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Academic literature on the topic 'Hypoxia regulators'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "Hypoxia regulators"

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Barth, Dominik A., Felix Prinz, Julia Teppan, Katharina Jonas, Christiane Klec, and Martin Pichler. "Long-Noncoding RNA (lncRNA) in the Regulation of Hypoxia-Inducible Factor (HIF) in Cancer." Non-Coding RNA 6, no. 3 (July 6, 2020): 27. http://dx.doi.org/10.3390/ncrna6030027.

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Hypoxia is dangerous for oxygen-dependent cells, therefore, physiological adaption to cellular hypoxic conditions is essential. The transcription factor hypoxia-inducible factor (HIF) is the main regulator of hypoxic metabolic adaption reducing oxygen consumption and is regulated by gradual von Hippel-Lindau (VHL)-dependent proteasomal degradation. Beyond physiology, hypoxia is frequently encountered within solid tumors and first drugs are in clinical trials to tackle this pathway in cancer. Besides hypoxia, cancer cells may promote HIF expression under normoxic conditions by altering various upstream regulators, cumulating in HIF upregulation and enhanced glycolysis and angiogenesis, altogether promoting tumor proliferation and progression. Therefore, understanding the underlying molecular mechanisms is crucial to discover potential future therapeutic targets to evolve cancer therapy. Long non-coding RNAs (lncRNA) are a class of non-protein coding RNA molecules with a length of over 200 nucleotides. They participate in cancer development and progression and might act as either oncogenic or tumor suppressive factors. Additionally, a growing body of evidence supports the role of lncRNAs in the hypoxic and normoxic regulation of HIF and its subunits HIF-1α and HIF-2α in cancer. This review provides a comprehensive update and overview of lncRNAs as regulators of HIFs expression and activation and discusses and highlights potential involved pathways.

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Cummins, Eoin P., and Cormac T. Taylor. "Hypoxia and inflammation." Biochemist 39, no. 4 (August 1, 2017): 34–36. http://dx.doi.org/10.1042/bio03904034.

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Uncontrolled or non-resolving inflammation is central to the pathophysiology of clinically important conditions including inflammatory bowel disease (IBD), psoriasis, atherosclerosis and arthritis. A combination of increased oxygen demand and decreased supply renders the local microenvironment of chronically inflamed tissues oxygen deprived (hypoxic), leading to the expression of a programme of genes that promote adaptation to the hypoxic challenge. This ancient and ubiquitous adaptive transcriptional pathway is governed by a transcription factor termed the hypoxia-inducible factor (HIF). Originally identified in the search for regulators of hypoxia-induced erythropoietin expression and adaptation to high altitude, HIF has been more recently recognized as a major regulator of immune cell function, which is central to the control of immunity and inflammation. Indeed, recent studies have demonstrated that the use of drugs targeting the HIF pathway may be of benefit in the treatment of chronic inflammatory disease.

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Stichternoth, Catrin, and Joachim F. Ernst. "Hypoxic Adaptation by Efg1 Regulates Biofilm Formation by Candida albicans." Applied and Environmental Microbiology 75, no. 11 (April 3, 2009): 3663–72. http://dx.doi.org/10.1128/aem.00098-09.

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ABSTRACT Hypoxia is encountered frequently by Candida albicans during systemic infection of the human host. We tested if hypoxia allows biofilm formation by C. albicans, which is a major cause of perseverance and antifungal resistance in C. albicans infections. Using an in vitro biofilm system, we unexpectedly discovered that several positive regulators of biofilm formation during normoxia, including Tec1, Ace2, Czf1, Och1, and Als3, had little or no influence on biofilm development during hypoxia, irrespective of the carbon dioxide level, indicating that C. albicans biofilm pathways differ depending on the oxygen level. In contrast, the Efg1 and Flo8 regulators were required for both normoxic and hypoxic biofilm formation. To explore the role of Efg1 during hypoxic and/or biofilm growth, we determined transcriptome kinetics following release of EFG1 expression by a system under transcriptional control of a doxycycline-inducible promoter. During hypoxia, Efg1 rapidly induced expression of all major classes of genes known to be associated with normoxic biofilm formation, including genes involved in glycolysis, sulfur metabolism, and antioxidative and peroxisome activities, as well as genes for iron uptake. The results suggest that hypoxic adaptation mediated by the Efg1 and Flo8 regulators is required even during normoxic biofilm development, while hypoxic biofilm formation in deep tissues or in organs may generate foci of C. albicans infections.

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Womeldorff, Matthew, David Gillespie, and Randy L. Jensen. "Hypoxia-inducible factor–1 and associated upstream and downstream proteins in the pathophysiology and management of glioblastoma." Neurosurgical Focus 37, no. 6 (December 2014): E8. http://dx.doi.org/10.3171/2014.9.focus14496.

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Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with an exceptionally poor patient outcome despite aggressive therapy including surgery, radiation, and chemotherapy. This aggressive phenotype may be associated with intratumoral hypoxia, which probably plays a key role in GBM tumor growth, development, and angiogenesis. A key regulator of cellular response to hypoxia is the protein hypoxia-inducible factor–1 (HIF-1). An examination of upstream hypoxic and nonhypoxic regulation of HIF-1 as well as a review of the downstream HIF-1–regulated proteins may provide further insight into the role of this transcription factor in GBM pathophysiology. Recent insights into upstream regulators that intimately interact with HIF-1 could provide potential therapeutic targets for treatment of this tumor. The same is potentially true for HIF-1–mediated pathways of glycolysis-, angiogenesis-, and invasion-promoting proteins. Thus, an understanding of the relationship between HIF-1, its upstream protein regulators, and its downstream transcribed genes in GBM pathogenesis could provide future treatment options for the care of patients with these tumors.

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Bracken, C. P., M. L. Whitelaw, and D. J. Peet. "The hypoxia-inducible factors: key transcriptional regulators of hypoxic responses." Cellular and Molecular Life Sciences (CMLS) 60, no. 7 (July 1, 2003): 1376–93. http://dx.doi.org/10.1007/s00018-003-2370-y.

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Lu, Xin, and Yibin Kang. "Hypoxia and Hypoxia-Inducible Factors: Master Regulators of Metastasis." Clinical Cancer Research 16, no. 24 (October 20, 2010): 5928–35. http://dx.doi.org/10.1158/1078-0432.ccr-10-1360.

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Li, Xiaochen, Yuanzhou He, Yongjian Xu, Xiaomin Huang, Jin Liu, Min Xie, and Xiansheng Liu. "KLF5 mediates vascular remodeling via HIF-1α in hypoxic pulmonary hypertension." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 4 (February 15, 2016): L299—L310. http://dx.doi.org/10.1152/ajplung.00189.2015.

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Hypoxic pulmonary hypertension (HPH) is characterized by active vasoconstriction and profound vascular remodeling. KLF5, a zinc-finger transcription factor, is involved in the excessive proliferation and apoptotic resistance phenotype associated with monocrotaline-induced pulmonary hypertension. However, the molecular mechanisms of KLF5-mediated pathogenesis of HPH are largely undefined. Adult male Sprague-Dawley rats were exposed to normoxia or hypoxia (10% O2) for 4 wk. Hypoxic rats developed pulmonary arterial remodeling and right ventricular hypertrophy with significantly increased right ventricular systolic pressure. The levels of KLF5 and hypoxia-inducible factor-1α (HIF-1α) were upregulated in distal pulmonary arterial smooth muscle from hypoxic rats. The knockdown of KLF5 via short-hairpin RNA attenuated chronic hypoxia-induced hemodynamic and histological changes in rats. The silencing of either KLF5 or HIF-1α prevented hypoxia-induced (5%) proliferation and migration and promoted apoptosis in human pulmonary artery smooth muscle cells. KLF5 was immunoprecipitated with HIF-1α under hypoxia and acted as an upstream regulator of HIF-1α. The cell cycle regulators cyclin B1 and cyclin D1 and apoptosis-related proteins including bax, bcl-2, survivin, caspase-3, and caspase-9, were involved in the regulation of KLF5/HIF-1α-mediated cell survival. This study demonstrated that KLF5 plays a crucial role in hypoxia-induced vascular remodeling in an HIF-1α-dependent manner and provided a better understanding of the pathogenesis of HPH.

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Catrina, Sergiu-Bogdan, and Xiaowei Zheng. "Hypoxia and hypoxia-inducible factors in diabetes and its complications." Diabetologia 64, no. 4 (January 26, 2021): 709–16. http://dx.doi.org/10.1007/s00125-021-05380-z.

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AbstractHypoxia-inducible factors (HIFs) are the key regulators of oxygen homeostasis in response to hypoxia. In diabetes, multiple tissues are hypoxic but adaptive responses to hypoxia are impaired due to insufficient activation of HIF signalling, which results from inhibition of HIF-1α stability and function due to hyperglycaemia and elevated fatty acid levels. In this review, we will summarise and discuss current findings about the regulation of HIF signalling in diabetes and the pathogenic roles of hypoxia and dysregulated HIF signalling in the development of diabetes and its complications. The therapeutic potential of targeting HIF signalling for the prevention and treatment of diabetes and related complications is also discussed. Graphical abstract

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Kabakov, Alexander E., and Anna O. Yakimova. "Hypoxia-Induced Cancer Cell Responses Driving Radioresistance of Hypoxic Tumors: Approaches to Targeting and Radiosensitizing." Cancers 13, no. 5 (March 4, 2021): 1102. http://dx.doi.org/10.3390/cancers13051102.

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Within aggressive malignancies, there usually are the “hypoxic zones”—poorly vascularized regions where tumor cells undergo oxygen deficiency through inadequate blood supply. Besides, hypoxia may arise in tumors as a result of antiangiogenic therapy or transarterial embolization. Adapting to hypoxia, tumor cells acquire a hypoxia-resistant phenotype with the characteristic alterations in signaling, gene expression and metabolism. Both the lack of oxygen by itself and the hypoxia-responsive phenotypic modulations render tumor cells more radioresistant, so that hypoxic tumors are a serious challenge for radiotherapy. An understanding of causes of the radioresistance of hypoxic tumors would help to develop novel ways for overcoming this challenge. Molecular targets for and various approaches to radiosensitizing hypoxic tumors are considered in the present review. It is here analyzed how the hypoxia-induced cellular responses involving hypoxia-inducible factor-1, heat shock transcription factor 1, heat shock proteins, glucose-regulated proteins, epigenetic regulators, autophagy, energy metabolism reprogramming, epithelial–mesenchymal transition and exosome generation contribute to the radioresistance of hypoxic tumors or may be inhibited for attenuating this radioresistance. The pretreatments with a multitarget inhibition of the cancer cell adaptation to hypoxia seem to be a promising approach to sensitizing hypoxic carcinomas, gliomas, lymphomas, sarcomas to radiotherapy and, also, liver tumors to radioembolization.

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Titova, O. N., N. A. Kuzubova, and E. S. Lebedeva. "The role of the hypoxia signaling pathway in cellular adaptation to hypoxia." Russian Medical Inquiry 4, no. 4 (2020): 207–13. http://dx.doi.org/10.32364/2587-6821-2020-4-4-207-213.

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The review presents an analysis of scientific publications in recent years devoted to the study on the cellular-molecular mechanism of cellular adaptation to hypoxia. In many respiratory diseases (chronic obstructive pulmonary disease, chronic respiratory failure, etc.), the balance between the cells’ need for oxygen and its delivery is disrupted. It complicates the course of the diseases and is a potential factor in their progression. The microenvironment in the inflammatory areas becomes hypoxic (so-called inflammatory hypoxia). The formation of long-term adaptation to pathological hypoxia is associated with the expression of a specific hypoxia-induced factor (HIF). It serves as a transcription activator for more than 300 genes and is a key regulator of various cellular and systemic responses to hypoxia, including angiogenesis, cell proliferation, cellular migration, regeneration, antigen presentation, cytokine and antimicrobial peptide production, phagocytosis, apoptosis, and cellular metabolic reprogramming. The article also considers the complex cross-interaction between HIF signaling and the nuclear transcription factor κB — NF-κB) signaling pathway (one of the main regulators of inflammation and immune responses). Possible therapeutic methods for controlling inflammation and immune-related diseases based on the principle of regulating the HIF signaling pathway are discussed. KEYWORDS: respiratory diseases, hypoxia, hypoxia-induced factor, adaptation, inflammation, immunity, targeted therapy. FOR CITATION: Titova O.N., Kuzubova N.A., Lebedeva E.S. The role of the hypoxia signaling pathway in cellular adaptation to hypoxia. Russian Medical Inquiry. 2020;4(4):207–213. DOI: 10.32364/2587-6821-2020-4-4-207-213.

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Dissertations / Theses on the topic "Hypoxia regulators"

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Gurevich, Rhonna Michelle. "Molecular regulators of hypoxia mediated apoptosis in ventricular myocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0023/MQ51721.pdf.

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Kolodziejski, Jakub. "Twist proteins as oxidative and hypoxic stress regulators." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTS008/document.

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Les facteurs de transcription Twist1 et Twist2 (famille Twist) jouent un rôle majeur dans le développement embryonnaire et dans la progression tumorale. Leur potentiel oncogénique dérive directement de la combinaison de leurs nombreuses activités développementales. Les gènes Twist peuvent notamment, en induisant la transition épithélio-mésenchymateuse (EMT), promouvoir l’invasion des cellules cancéreuses et participer de ce fait aux processus métastatique. De plus, en bloquant l’activité des voies de signalisation Rb et p53, ils peuvent inhiber les deux principaux programmes de sauvegarde cellulaire que sont l’apoptose et la senescence. Enfin, ils sont également impliqués dans la résistance des cellules cancéreuses aux agents chimio-thérapeutiques. En plus de ces nombreuses activités, nos données préliminaires nous ont amené à considérer un rôle de Twist dans la réponse au stress. Les cellules cancéreuses doivent croitre dans un environnement en perpétuel changement qui génère de nombreux types de stress. Seules les cellules capables de s’adapter, peuvent survivre et acquérir de nouvelles capacités les rendant plus agressives. La résistance au stress fait donc partie intégrante de la progression tumorale. Nos travaux révèlent que Twist en induisant une résistance au stress, plus particulièrement métabolique, est un acteur essentiel de l’acquisition d’u phénotype agressif des cellules cancéreuses. Dans une première étude, nous avons montré que Twist module le stress oxydatif, une condition très fréquemment retrouvée dans les tumeurs. Ainsi, nos résultats indiquent que l’expression de Twist provoque une réduction du taux d’espèces réactives de l’oxygène (ROS) intracellulaire. Cette activité a pour conséquence directe d’induire une résistance accrue à l’apoptose déclenchée par divers traitements. Nous avons par la suite caractérisé cette activité et mis en évidence un programme génétique contrôlé par Twist impliquant divers facteurs possédant des propriétés anti-oxydantes. Dans un second temps, nous nous sommes intéressés à un autre type de stress métabolique, l’hypoxie. L’hypoxie définie par un taux insuffisant d’oxygène, est retrouvée dans la plupart des tumeurs solides du fait de l’absence ou de l’anomalité de la vascularisation. L’hypoxie mène à la stabilisation d’un facteur de transcription, HIF1α. Cette protéine est essentielle à l’adaptation hypoxique et contrôle l’expression de nombreux gènes impliqués dans le métabolisme du glucose, le transport de l’oxygène, l’angiogenèse ou l’apoptose. Dans les premiers temps d’hypoxie, l’effet d’adaptation induit par HIF1α est bénéfique pour les cellules. Cependant, si l’absence d’oxygène se prolonge, HIF1α, peut pousser les cellules vers la mort. Nos travaux démontrent que Twist est capable de rendre les cellules résistantes à une hypoxie prolongée. De plus, cette activité de protection contre le stress hypoxique agit via un effet paracrine. Enfin, nos données suggèrent que cet effet est médié par une interaction directe entre les protéines Twist et HIF1α. Au final, cette étude indique que l’expression de Twist dans les cellules cancéreuses, en conférant une résistance accrue à l’environnement hypoxique, joue un rôle essentiel dans l’adaptation au stress et à l’acquisition de nouveaux phénotypes agressifs. En résumé, L’objectif principal de ma thèse était de mettre en évidence de nouvelles propriétés cellulaires des oncogènes de la famille Twist. Nos résultats démontrent que Twist par ses capacités à contrôler le stress métabolique, permet à la cellule cancéreuse de mieux s’adapter et donc survivre dans un environnement en constante évolution. Nos travaux renforcent donc la notion de l’importance de ces facteurs dans la progression tumorale
Twist1 and Twist2 are related transcription factors that play major roles both during embryonic development and in several pathologies, including cancer. Twists' oncogenic potential arises from a combination of their multiple functions in development. Notably, both Twist induce epithelial-to mesenchymal transition, thus promoting tumour invasiveness and possibly conferring to cells self-renewal properties. Furthermore, through disruption of both Rb- and p53-driven pathways, Twist override two major oncogene-induced fail-safe programs, namely senescence and apoptosis, thereby promoting malignant conversion. Twist has also been reported to participate in acquisition of drug resistance and in promotion of neo-angiogenesis.Current knowledge of pleiotropic activities of Twist prompted us to postulate that these factors may be major regulators of stress response. Cancer cells survive and grow within a continuously changing environment that creates multiple stresses to which they must adapt in order to survive and strive. Such adaptations often give rise to the acquisition of an aggressive phenotype. Consistent with this hypothesis, we recently unveiled new activities of Twist proteins that are related to stress response. We have shown that Twist regulates response to oxidative stress, a condition exacerbated in cancer by stimuli such as inflammation, increased cellular metabolism and changes in tumour oxygenation. Our work has contributed to the understanding of molecular mechanisms through which Twist diminishes cellular ROS and thus participates in the escape from apoptosis and senescence. In the first part of my thesis, I worked on the antioxidant activity of Twist and described its molecular mechanisms.The second part of my work addressed the impact of Twist proteins on cellular response to hypoxia that is insufficient oxygen supply, frequently found in solid tumours. Cellular response to hypoxic stress relies on stabilization and activation of HIF1α, a key transcriptional mediator of the hypoxic response, regulating numerous genes involved in glucose metabolism, oxygen transport, angiogenesis, cell growth and apoptosis. HIF1α is beneficial for cancer cells in response to short hypoxic episodes, however its sustained activation in case of prolonged hypoxia may push cancer cells towards apoptosis. In this context, we have shown that Twist protects cancer cells from hypoxia-induced apoptosis. We have discovered HIF1α and Twist physically interact, suggesting a possible mechanistic basis for Twist's protective effect. These results led us to postulate that Twist plays a role in cellular response to hypoxia and thus participates in cancer cell adaptation and acquisition of aggressive phenotypes triggered by lack of oxygen.Our results reinforce the notion that Twist factors are major cellular stress modulators that might be important for adaptation of cancer cells to changing conditions in the process of tumour progression

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White, Carine Petris Michael J. "Inflammation and hypoxia novel regulators of mammalian copper homeostasis in macrophages /." Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/6624.

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Title from PDF of title page (University of Missouri--Columbia, viewed on March 8, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Michael J. Petris. Vita. Includes bibliographical references.

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Peurala, E. (Emmi). "Regulators of hypoxia response and the cell cycle in breast cancer." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526202709.

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Abstract Breast cancer is the most common cancer affecting the female population of the Western world. It is a heterogeneous disease entity that encompasses tumors with remarkably different forms of behaviour, and it is therefore vital to distinguish patients with good and poor prognoses. The classical prognostic and predictive factors for breast cancer serve as tools for clinical oncologists when planning treatment, but the growing awareness of breast cancer biology is bringing about a need for novel prognostic and predictive biomarkers. This thesis examines the prognostic significance of hypoxia response and cell cycle regulators in ductal breast cancer and in triple-negative breast cancer (negative for hormone receptors and human epidermal growth factor receptor 2), concluding that PHD2 and PHD3 are associated with a good prognosis, while the role of PHD1 is controversial, as it is associated with proliferation in ductal breast cancer but with node-negative status in triple-negative breast cancer. In our experiments HIF-1α redeemed its role as a marker of an adverse prognosis, whereas the role of HIF-2α appeared to be the opposite. Our data suggest that PHDs can have other targets than the HIF-αs, and that triple-negative breast tumors express more HIF-1α and less HIF-2α and PHD3 than those with a good prognosis. Furthermore, we identified cyclin D1 as a biomarker with independent prognostic significance in ductal breast cancer, being associated with good prognostic factors and a better outcome, whereas the opposite was seen in triple-negative breast cancer. CDK4 was associated with high proliferation in triple-negative breast cancer. In addition, high levels of p16 correlated with increased survival in breast cancer patients independently of receptor status
Tiivistelmä Rintasyöpä on naisten yleisin syöpä läntisessä maailmassa. Rintasyöpä on heterogeeninen tautiryhmä, jossa kasvaimet vaihtelevat biologiselta käyttäytymiseltään huomattavasti. Tästä syystä on tärkeää erottaa hyvä- ja huonoennusteiset potilaat. Syöpälääkärit käyttävät klassisia ennustetekijöitä hoitopäätöksiä tehdessään, mutta lisääntynyt tieto rintasyövän biologiasta on saanut aikaan tarpeen löytää uusia ennustetekijöitä. Tässä väitöskirjatyössä tutkimme hypoksiavasteen ja solusyklin säätelijöiden ennusteellisuutta duktaalisessa rintasyövässä sekä kolmoisnegatiivisessa (ei ilmennä hormonireseptoreita eikä epidermaalikasvutekijäreseptoria) rintasyövässä. PHD2 ja PHD3:n vahva ilmentyminen liittyi parempaan ennusteeseen, mutta PHD1:n esiintymisen vaikutus oli ristiriitainen. PHD1:n ilmentyminen liittyi lisääntyneeseen solujakautumiseen duktaalisessa rintasyövässä, mutta kolmoisnegatiivisessa rintasyövässä sen esiintyminen liittyi vähentyneeseen imusolmukemetastasointiin. Tutkimuksessamme HIF-1α osoittautui huonon ennusteen merkiksi. Sitä vastoin HIF-2α:n ilmentymisen vaikutus näytti liittyvän parempaan ennusteeseen. Tuloksemme osoittavat, että PHD-entsyymeillä on mahdollisesti muitakin kohteita kuin HIF-α:t. Osoitimme myös, että HIF-1α:n ilmentyminen on yleisempää ja HIF-2α:n sekä PHD3:n ilmentyminen vähäisempää kolmoisnegatiivisessa kuin duktaalisessa rintasyövässä. Lisäksi totesimme, että sykliini D1 on itsenäinen ennustetekijä liittyen parempaan ennusteeseen duktaalisessa rintasyövässä. Huomioitavaa on kuitenkin, että kolmoisnegatiivisessa rintasyövän alaryhmässä sykliini D1:n esiintyminen oli huonon ennusteen merkki. CDK4 osoittautui voimakkaan proliferaation merkiksi kolmoisnegatiivisessa rintasyövässä. Lisäksi osoitimme, että p16:n ilmentyminen liittyy parempaan ennusteeseen sekä duktaalisessa rintasyövässä että kolmoisnegatiivisessa rintasyövässä

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Catrina, Sergiu-Bogdan. "Regulators of angiogenesis in diabetes and tumors /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-628-6682-6/.

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Camus, Victoria Louise. "Investigating the effects of chemotherapy and radiation therapy in a prostate cancer model system using SERS nanosensors." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25386.

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Intracellular redox potential (IRP) is a measure of how oxidising or reducing the environment is within a cell. It is a function of numerous factors including redox couples, antioxidant enzymes and reactive oxygen species. Disruption of the tightly regulated redox status has been linked to the initiation and progression of cancer. However, there is very limited knowledge about the quantitative nature of the redox potential and pH gradients that exist in cancer tumour models. Multicellular tumour spheroids (MTS) are three-dimensional cell cultures that possess their own microenvironments, similar to those found in tumours. From the necrotic core to the outer proliferating layer there exist gradients of oxygen, lactate, pH and drug penetration. Tumours also have inadequate vasculature resulting in a state of hypoxia. Hypoxia is a key player in metabolic dysregulation but can also provide cells with resistance against cancer treatments, particularly chemotherapy and radiation therapy. The primary hypoxia regulators are HIFs (Hypoxia Inducible Factors) which under low O2 conditions bind a hypoxia response element, inhibiting oxidative phosphorylation and upregulating glycolysis which has two significant implications: the first is an increase in levels of NADPH/NADH, the main electron donors found in cells which impacts the redox state, whilst the second is a decrease in intracellular pH (pHi) because of increased lactate production. Thus, redox state and intracellular pHi can be used as indicators of metabolic changes within 3D cultures and provide insight into cellular response to therapy. Surface-Enhanced Raman Spectroscopy (SERS) provides a real-time, high resolution method of measuring pHi and IRP in cell culture. It allows for quick and potentially portable analysis of MTS, providing a new platform for monitoring response to drugs and therapy in an unobtrusive manner. Redox and pH-active probes functionalised to Au nanoshells were readily taken up by prostate cancer cell lines and predominantly found to localise in the cytosol. These probes were characterised by density functional theory and spectroelectrochemistry, and their in vitro behaviour modelled by the chemical induction of oxidative and reductive stress. Next, targeting nanosensors to different zones of the MTS allowed for spatial quantification of redox state and pHi throughout the structure and the ability to map the effects of drug treatments on MTS redox biology. The magnitude of the potential gradient can be quantified as free energy (ΔG) and used as a measurement of MTS viability. Treatment of PC3 MTS with staurosporine, an apoptosis inducer, was accompanied by a decrease in free energy gradients over time, whereas treatment of MTS with cisplatin, a drug to which they are resistant, showed an increase in viability indicating a compensatory mechanism and hence resistance. Finally, using this technique the effects of ionising radiation on IRP and pHi in the tumour model was explored. Following exposure to a range of doses of x-ray radiation, as well as single and multi-fractionated regimes, IRP and pHi were measured and MTS viability assessed. Increased radiation dosage diminished the potential gradient across the MTS and decreased viability. Similarly, fractionation of a single large dose was found to enhance MTS death. This novel SERS approach therefore has the potential to not only be used as a mode of drug screening and tool for drug development, but also for pre-clinical characterisation of tumours enabling clinicians to optimise radiation regimes in a patient-specific manner.

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Guimbellot, Jennifer S. "Role of hypoxia in epithelial gene regulation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/guimbellot.pdf.

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REYNOLDS, PAUL R. "MIDKINE (MK) REGULATES PULMONARY VASCULAR REMODELING DURING HYPOXIA." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1085492908.

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Hsu, Fu-Chiun. "Construction of transcriptional regulatory pathways associated with hypoxia in Arabidopsis." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/1231.

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Transcriptional control plays a major role in regulating hypoxic responses in plants. However, the transcriptional regulatory networks associated with hypoxia remain to be constructed. By transcriptomic analysis I show here that a novel systemic transcriptional reprogramming, which is mediated via the interplay of hormones, facilitates the survival of plants under flooding. A feasible strategy for identifying downstream targets of transcription factors (TFs) was developed. The downstream pathways of a hypoxia-responsive TF, WRKY22, were constructed. The results also show that AtERF73/HRE1 (Arabidopsis thaliana Ethylene Response Factor 73/Hypoxia Responsive ERF 1) modulate ethylene-dependent and -independent responses during hypoxia. Transcriptomic analysis of Arabidopsis in both root and shoot tissues during flooding of roots indicates the existence of a systemic communication through transcriptional reprogramming. By functional classification of affected genes, a comprehensive managing program of carbohydrate metabolism was observed. Through transcriptional profiling in ethylene and abscisic acid (ABA) signaling mutants, ein2-5 and abi4-1, an alteration of long-distance hypoxic regulation was uncovered in ein2-5 and abi4-1. Moreover, genes involved in ABA biosynthesis were also found to be differentially regulated between shoots and roots. Many members of the WRKY TF family were highly induced by hypoxia. One of the early-induced WRKYs, WRKY22, which has the highest induced level, was chosen for identifying its downstream targets. Anoxic tolerance was affected in WRKY22 overexpressing (WRKY22-OX) and knock-out (wrky22-ko) lines. Comparison of differential gene expression profiles between the wild-type and WRKY22-OX and between the wild-type and wrky22-ko lines by microarray analysis identified novel hypoxia-responsive genes as WRKY22 targets. Chromatin immunoprecipitation (ChIP) followed by microarray hybridization (ChIP-chip) and ChIP followed by quantitative PCR (ChIP-qPCR) were utilized to analyze in vivo interactions. To study the role of ethylene during hypoxia, I characterized an AP2/ERF (APETALA2/ethylene response factor) AtERF73/HRE1 that is specifically induced during hypoxia. I showed that the expression of AtERF73/HRE1 can be induced by exogenous 1-aminocyclopropane-1-carboxylic acid (ACC), a precursor of ethylene. Its hypoxic induction was reduced but not completely abolished in ethylene-insensitive mutants and in the presence of inhibitors of ethylene biosynthesis and responses. Increased ethylene sensitivity and exaggerated triple responses were observed in HRE1-RNAi knock-down lines. By comparing expression differences between the wild-type and HRE1-RNAi lines, I found that hypoxic induction of glycolytic and fermentative genes was reduced by the HRE1-RNAi knock-down mutations, whereas induction of a number of peroxidase and cytochrome P450 genes was increased. Collectively, these results show that AtERF73/HRE1 is involved in modulating ethylene responses under both normoxia and hypoxia.

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Batie, Michael. "Role of chromatin structure and JmjC histone demethylases in the response to hypoxia." Thesis, University of Dundee, 2017. https://discovery.dundee.ac.uk/en/studentTheses/ce1fbbd7-d3be-49c2-a89e-46b739236887.

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In response to low oxygen (hypoxia), cells have evolved sophisticated gene expression programmes for survival and adaption. How the chromatin state coordinates these changes remains largely unknown. Global histone methylation changes occur in response to hypoxia, however, temporal dynamics of histone methylation changes and how they correlate with hypoxia induced gene transcription changes is ill defined. The Jumonji C (Jmjc) histone demethylases are oxygen dependent enzymes and represent a potential link between chromatin structure and oxygen sensing. Many of these enzymes are differentially expressed in hypoxia and some have been found to influence the hypoxic response. Here, the JmjC histone demethylase, KDM2B, is found to be induced at the mRNA level but not at the protein level in response to hypoxia. KDM2B was also found to regulate the transcriptional response hypoxia, in a cell type dependent manner, through control of Hypoxia Inducible Factor (HIF) subunits, HIF 1 and 2α. These findings highlight complex HIF-KDM2B crosstalk involved in the cells response to low oxygen. Additionally, it was found that various histone methylation marks are induced in the early response to hypoxia prior to hypoxia induced gene transcription changes. This demonstrates that chromatin structural marks responds rapidly to changes in oxygen availability. Furthermore the methylation landscape of 2 two active transcription histone methylation marks, H3K4me3 and H3K36me3, were mapped by ChIP sequencing in the acute response to hypoxia. This analyses found specific changes in histone methylation, which correlate with the core gene transcription changes in hypoxia, pointing towards a mechanism by which rapid chromatin changes programs the cell for hypoxic transcription. Finally, KDM5A was identified to, at least in part, regulate early hypoxia H3K4me3 changes and changes in gene expression of a subset of hypoxia responsive genes. Findings described herein provide evidence for the role of chromatin structure dynamics, mediated by chromatin modifying enzymes, in regulating the hypoxic response. Specifically, early histone methylation changes elicited in acute hypoxia may help establish a chromatin landscape for the cell to transcriptionally respond, which is essential for survival and adaptation to hypoxia. Insights into chromatin dynamics in the response to hypoxia and the role played by JmjC histone demethylases in regulating the hypoxic response has the potential for new drug discovery in diseases such as cancer, were hypoxia, epigenetics and JmjC enzymes are often implicated in disease progression.

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Books on the topic "Hypoxia regulators"

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Jamie, Goode, Chadwick Derek, Novartis Foundation, and Symposium on the Tumour Microenvironment: Causes and Consequences of Hypoxia and Acidity (2000 : London, England), eds. The tumour microenvironment: Causes and consequences of hypoxia and acidity. Chichester: Wiley, 2001.

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The Tumour Microenvironment - No. 240: Causes and Consequences of Hypoxia and Acidity (Novartis Foundation Symposia). Wiley, 2001.

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Book chapters on the topic "Hypoxia regulators"

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Acker, Till, and Karl H. Plate. "Hypoxia and Hypoxia Inducible Factors (HIF) as Important Regulators of Tumor Physiology." In Cancer Treatment and Research, 219–48. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8871-3_14.

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Imtiyaz, Hongxia Z., and M. Celeste Simon. "Hypoxia-Inducible Factors as Essential Regulators of Inflammation." In Current Topics in Microbiology and Immunology, 105–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_74.

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Ahmad, Aftab, Carl W. White, and Shama Ahmad. "Hypoxia-Inducible Factors and Adenosine Signaling in Vascular Growth." In Extracellular ATP and Adenosine as Regulators of Endothelial Cell Function, 113–24. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3435-9_7.

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Watt, Suzanne M., Grigorios Tsaknakis, Sinead P. Forde, and Lee Carpenter. "Stem Cells, Hypoxia and Hypoxia-Inducible Factors." In Regulatory Networks in Stem Cells, 211–31. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-227-8_18.

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Mkrtchian, Souren, Kian Leong Lee, Jessica Kåhlin, Anette Ebberyd, Lorenz Poellinger, Malin Jonsson Fagerlund, and Lars I. Eriksson. "Hypoxia Regulates MicroRNA Expression in the Human Carotid Body." In Advances in Experimental Medicine and Biology, 25–33. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91137-3_3.

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Abraham, R. T. "mTOR as a Positive Regulator of Tumor Cell Responses to Hypoxia." In Current Topics in Microbiology and Immunology, 299–319. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18930-2_18.

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Conrad, P. William, David E. Millhorn, and Dana Beitner-Johnson. "Hypoxia Differentially Regulates the Mitogen- and Stress-Activated Protein Kinases." In Oxygen Sensing, 293–302. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46825-5_28.

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Mishra, Aastha, and M. A. Qadar Pasha. "HIF-1 and EGLN1 Under Hypobaric Hypoxia: Regulation of Master Regulator Paradigm." In Translational Research in Environmental and Occupational Stress, 81–91. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1928-6_8.

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Gerasimovskaya, Evgenia V., Kurt R. Stenmark, and Gennady G. Yegutkin. "Role of Purine-Converting Ecto-Enzymes in Angiogenic Phenotype of Pulmonary Artery Adventitial Vasa Vasorum Endothelial Cells of Chronically Hypoxic Calves." In Extracellular ATP and Adenosine as Regulators of Endothelial Cell Function, 73–93. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3435-9_5.

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Hochachka, P. W. "Metabolic Key to Hypoxia Tolerance: Loss of Regulatory Links Between the Electron Transfer System and Glycolysis." In Integration of Mitochondrial Function, 623–27. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2551-0_60.

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Conference papers on the topic "Hypoxia regulators"

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Yang, Chunzhang, Herui Wang, Karel Pacak, and Zhengping Zhuang. "Abstract 3943: Genetic abnormalites in hypoxia sensing regulators cause human pheochromocytoma/paraganglioma and plolycythemia syndrome." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3943.

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Kingston, John, Geoffrey Grandjean, Geoffrey Bartholomeusz, Brian P. James, Laura Gumbiner-Russo, Mei Koh, and Garth Powis. "Abstract 5505: A genome-wide siRNA screen for novel regulators of HIF-1α activity in normoxia and hypoxia." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5505.

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Oppegard, Shawn C., and David T. Eddington. "Modulation of Oxygen Tensions via Microfabricated Devices." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53093.

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Oxygen is a key modulator of many cellular pathways and plays an important role in a number of cellular behaviors. The hypoxic inducible factor 1α (HIF-1α) is often considered the master regulator of the cellular response to oxygen tension (1). HIF-1α is a transcription factor involved in angiogenesis, glucose transport and glycolysis, apoptosis, migration, and differentiation, among many other functions (2). Unfortunately devices permitting in vitro oxygen modulation fail to meet the needs of biomedical research due to the inability to effectively mimic conditions found in vivo. The gold standard for hypoxia work is the hypoxic chamber, but the tool requires hours for equilibration and is not effective at generating very low oxygen levels (3). As an example demonstrating this disadvantage, cancer tumor oxygenation can change in the span of minutes (4). Intermittent hypoxia, or the changing of oxygen over time, has been shown to be important in heart attack, stroke, and sleep apnea as well. Other microfluidic approaches, although offering more oxygen control, are often difficult to disseminate to other labs due to the requirement of specialized methods and equipment for their operation. In this work, a microfabricated technology has been developed to grant precise control the temporal and spatial oxygen concentration exposed to both cell monolayers in the multiwell plate as well as with 3-D cell-seeded constructs. The concept is adaptable to both pre-established and novel experiments depending on the needs of the researcher. The devices are simple to use and require minimal additional equipment beyond what is available to a standard cell culture lab.

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Li, J., S. Bevans-Fonti, LA Shimoda, GL Semenza, and VY Polotsky. "Hypoxia Up-Regulates Genes of Lipid Biosynthesis Via Hypoxia Inducible Factor 1 (HIF-1)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5333.

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Greville, Gordon, Esther Llop, Rosa Peracaula Miró, Amanda McCann, Pauline M. Rudd, and Radka Saldova. "Abstract 2423: Hypoxia regulates tumor cell invasiveness through altered glycosylation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2423.

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Das, Tuhin, Alexandra Pisklakova, Zhaoliang Fei, and Yulia Nefedova. "Abstract 1534: Hes1 regulates hypoxia induced chemoresistance of myeloma cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1534.

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Dabral, Swati, Christian Muecke, Chanil Valsarajan, Mario Schmoranzer, Astrid Wietelmann, Norbert Weissmann, Rajkumar Savai, Werner Seeger, Reinhard Dammann, and Soni Savai Pullamsetti. "RASSF1A regulates ROS-HIF axis in hypoxia driven pulmonary hypertension." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa3008.

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Gao, Xuefeng, Chwanrow K. Baban, Mark Tangney, and Sabin Tabirca. "Computer simulation of hypoxia regulates avascular tumor growth through p27 expression." In 2011 IEEE/ICME International Conference on Complex Medical Engineering - CME 2011. IEEE, 2011. http://dx.doi.org/10.1109/iccme.2011.5876697.

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Santhosh, K., S. Zhang, and S. Dakshinamurti. "Palmitoylation of Pulmonary Arterial Thromboxane Receptor Regulates Receptor Hyperresponsiveness in Hypoxia." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2479.

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Manzo, Nicholas D., and Barry R. Stripp. "Hypoxia Regulates The Clonogenic And Differentiation Potentials Of Airway Progenitor Cells." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6333.

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