Dynamic regulation of epigenetic demethylation by oxygen availability and cellular redox

Lamadema, Nermina; Burr, Simon; Brewer, Alison C.

doi:10.1016/j.freeradbiomed.2018.12.009

Cited by 41 publications

(31 citation statements)

References 273 publications

(258 reference statements)

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“…Chronic hypoxia also results in a change in gene expression that is not related to the activation of HIF and NF-κB but is related to changes in DNA and histone methylation [109]. A reduction in the amount of oxygen results in the decreased activity of the ten-eleven translocation protein (TET) and jumonji histone demethylases (JHDMs) [110,111], enzymes responsible for the demethylation of DNA and histones. Consequently, a hypoxia-induced increase in the methylation of DNA and histones leads to the reduced expression of many genes.…”

Section: Chronic Hypoxiamentioning

confidence: 99%

“…Its expression is regulated by chronic hypoxia via various mechanisms. Reduced oxygen levels decrease the activity of JHDMs [111], enzymes involved in histone demethylation, and thus hypoxia causes methylation of histones in the promoter of the CCR1 gene [149]. This results in a reduced CCR1 expression in macrophages and monocytes [144,149].…”

Section: Impact Of Hypoxia On Ccr1 Expressionmentioning

confidence: 99%

“…Chronic hypoxia is associated with a decrease in the activity of oxygen-dependent enzymes, for example, JHDMs [111]. The reduced activity of these enzymes leads to the methylation of the histones in the promoter and enhancer regions of the CCL2 gene [149,169], especially in the NF-κB binding sequence [149].…”

Section: Impact Of Hypoxia On Ccr1 Expressionmentioning

confidence: 99%

See 2 more Smart Citations

Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review

Korbecki

Kojder

Barczak

et al. 2020

IJMS

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Hypoxia, i.e., oxygen deficiency condition, is one of the most important factors promoting the growth of tumors. Since its effect on the chemokine system is crucial in understanding the changes in the recruitment of cells to a tumor niche, in this review we have gathered all the available data about the impact of hypoxia on β chemokines. In the introduction, we present the chronic (continuous, non-interrupted) and cycling (intermittent, transient) hypoxia together with the mechanisms of activation of hypoxia inducible factors (HIF-1 and HIF-2) and NF-κB. Then we describe the effect of hypoxia on the expression of chemokines with the CC motif: CCL1, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL15, CCL16, CCL17, CCL18, CCL19, CCL20, CCL21, CCL22, CCL24, CCL25, CCL26, CCL27, CCL28 together with CC chemokine receptors: CCR1, CCR2, CCR3, CCR4, CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10. To better understand the effect of hypoxia on neoplastic processes and changes in the expression of the described proteins, we summarize the available data in a table which shows the effect of individual chemokines on angiogenesis, lymphangiogenesis, and recruitment of eosinophils, myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and tumor-associated macrophages (TAM) to a tumor niche.

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Section: Chronic Hypoxiamentioning

confidence: 99%

Section: Impact Of Hypoxia On Ccr1 Expressionmentioning

confidence: 99%

See 1 more Smart Citation

Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review

Korbecki

Kojder

Barczak

et al. 2020

IJMS

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“…It is known that under graded levels of available O2 (0.5 to 5%) TET shows differential activity. These O2 concentrations can be expected in different developing tissues (Lamadema et al, 2019). In contrast to the described phenotype of the triple mutant in mice, in zebrafish the tripe mutant of tet1, tet2 and tet3 are able to advance further in gastrulation (Li et al, 2015) contrary to what can be expected from the observed effects of the triple TET mutants in mouse.…”

Section: Oxygen and Ros In Animal Developmentmentioning

confidence: 92%

Oxygen, reactive oxygen species and developmental redox networks: Evo-Devo Evil-Devils?

Salas‐Vidal¹,

Méndez-Cruz²,

Ramírez-Corona³

et al. 2021

Int. J. Dev. Biol.

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Molecular oxygen (O2), reactive oxygen species (ROS), and associated redox networks are cornerstones of aerobic life, these molecules and networks have gained recognition as fundamental players in mechanisms that regulate the development of multicellular organisms. First, we present a brief review in which we provide a historical description of some relevant discoveries that led to this recognition. We also discuss that despite its abundance in nature, oxygen is a limiting factor, and its high availability variation impacted the evolution of adaptive mechanisms to guarantee the proper development of diverse species under such extreme environments. Finally, some examples when oxygen and ROS were identified as relevant for the control of developmental processes are discussed. We take into account not only the current knowledge on animal redox developmental biology, but also briefly discuss potential scenarios on the origin and evolution of redox developmental mechanisms and the importance of the ever-changing environment.

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“…The bioavailability of Fe 2+ in vivo is determined by multiple mechanisms which regulate cellular redox and iron homeostasis (transport, storage and metabolism) which may all impact upon the activities of TETs and JmjCs [110]. In hyperglycaemia, the cellular redox balance becomes perturbed, favouring excessive production of reactive oxygen species (ROS) and overloading the antioxidant defences which usually counteract this (Fig.…”

Section: Hyperglycaemia and Metabolismmentioning

confidence: 99%

Dysregulation of 2-oxoglutarate-dependent dioxygenases by hyperglycaemia: does this link diabetes and vascular disease?

Green

Brewer

2020

Clin Epigenet

Self Cite

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The clinical, social and economic burden of cardiovascular disease (CVD) associated with diabetes underscores an urgency for understanding the disease aetiology. Evidence suggests that the hyperglycaemia associated with diabetes is, of itself, causal in the development of endothelial dysfunction (ED) which is recognised to be the critical determinant in the development of CVD. It is further recognised that epigenetic modifications associated with changes in gene expression are causal in both the initiation of ED and the progression to CVD. Understanding whether and how hyperglycaemia induces epigenetic modifications therefore seems crucial in the development of preventative treatments. A mechanistic link between energy metabolism and epigenetic regulation is increasingly becoming explored as key energy metabolites typically serve as substrates or co-factors for epigenetic modifying enzymes. Intriguing examples are the ten-eleven translocation and Jumonji C proteins which facilitate the demethylation of DNA and histones respectively. These are members of the 2-oxoglutarate-dependent dioxygenase superfamily which require the tricarboxylic acid metabolite, α-ketoglutarate and molecular oxygen (O 2) as substrates and Fe (II) as a co-factor. An understanding of precisely how the biochemical effects of high glucose exposure impact upon cellular metabolism, O 2 availability and cellular redox in endothelial cells (ECs) may therefore elucidate (in part) the mechanistic link between hyperglycaemia and epigenetic modifications causal in ED and CVD. It would also provide significant proof of concept that dysregulation of the epigenetic landscape may be causal rather than consequential in the development of pathology.

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Dynamic regulation of epigenetic demethylation by oxygen availability and cellular redox

Cited by 41 publications

References 273 publications

Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review

Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review

Oxygen, reactive oxygen species and developmental redox networks: Evo-Devo Evil-Devils?

Dysregulation of 2-oxoglutarate-dependent dioxygenases by hyperglycaemia: does this link diabetes and vascular disease?

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