Close teamwork between Nrf2 and peroxiredoxins 1 and 6 for the regulation of prostaglandin D2 and E2 production in macrophages in acute inflammation

Ishii, Tetsuro

doi:10.1016/j.freeradbiomed.2015.04.034

Cited by 38 publications

(28 citation statements)

References 108 publications

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“…Lipocalin prostaglandin D synthase (L-PGDS) is expressed in BAT where it has a key role in energy substrate utilization. It is also localized in the central nervous system and it is involved in inflammatory modulations amongst other functions (166). Deletion of L-PGDS leads to inadequate thermogenesis in BAT because of impairment in switching of substrate utilization from glucose to lipids (70, 167).…”

Section: Brown Adipocytes Secrete Pro/anti-inflammatory Mediatorsmentioning

confidence: 99%

Inflammatory Signaling and Brown Fat Activity

Omran

Christian

2020

Front. Endocrinol.

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Obesity is characterized by a state of chronic inflammation in adipose tissue mediated by the secretion of a range of inflammatory cytokines. In comparison to WAT, relatively little is known about the inflammatory status of brown adipose tissue (BAT) in physiology and pathophysiology. Because BAT and brown/beige adipocytes are specialized in energy expenditure they have protective roles against obesity and associated metabolic diseases. BAT appears to be is less susceptible to developing inflammation than WAT. However, there is increasing evidence that inflammation directly alters the thermogenic activity of brown fat by impairing its capacity for energy expenditure and glucose uptake. The inflammatory microenvironment can be affected by cytokines secreted by immune cells as well as by the brown adipocytes themselves. Therefore, pro-inflammatory signals represent an important component of the thermogenic potential of brown and beige adipocytes and may contribute their dysfunction in obesity.

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Section: Brown Adipocytes Secrete Pro/anti-inflammatory Mediatorsmentioning

confidence: 99%

Inflammatory Signaling and Brown Fat Activity

Omran

Christian

2020

Front. Endocrinol.

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“…There are three types of PGES (EC 5.3.99.3): two microsomal (mPGES1 and mPGES2) and one cytosolic (cPGES aka PGES3). These enzymes have different origin, different physiological properties, different cell localisation, regulation, and catalytic mechanisms, yet they are all involved in the synthesis of the same PG (127,128). Earlier it was believed that mPGES2 was glutathione-independent, in contrast to the rest of the PGESs, but recent research has confirmed that mPGES2 binding activity is possible only in the presence of glutathione (101).…”

Section: Prostaglandin E2 Synthasesmentioning

confidence: 99%

Glutathionylation: a regulatory role of glutathione in physiological processes

Dominko

Đikić

2018

Archives of Industrial Hygiene and Toxicology

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Glutathione (γ-glutamyl-cysteinyl-glycine) is an intracellular thiol molecule and a potent antioxidant that participates in the toxic metabolism phase II biotransformation of xenobiotics. It can bind to a variety of proteins in a process known as glutathionylation. Protein glutathionylation is now recognised as one of important posttranslational regulatory mechanisms in cell and tissue physiology. Direct and indirect regulatory roles in physiological processes include glutathionylation of major transcriptional factors, eicosanoids, cytokines, and nitric oxide (NO). This review looks into these regulatory mechanisms through examples of glutathione regulation in apoptosis, vascularisation, metabolic processes, mitochondrial integrity, immune system, and neural physiology. The focus is on the physiological roles of glutathione beyond biotransformational metabolism.

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“…15d PGJ2 is not only an Nrf2 activator acting through Keap1 binding [34] but is also a ligand for peroxisome proliferator-activated receptor gamma (PPAR-γ) which bears functional AREs for Nrf2 modulation [35]. Through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) inhibition, it is known as a key regulator of inflammation [36,37]. We also demonstrated Nrf2-dependent protection against ALI by 15d-PGJ2 in mice [35].…”

Section: Lincs Analysis For Chemical Targetsmentioning

confidence: 99%

Potential therapeutic targets in Nrf2-dependent protection against neonatal respiratory distress disease predicted by cDNA microarray analysis and bioinformatics tools

Cho

Wang

et al. 2016

Current Opinion in Toxicology

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Hyperoxia exposure of newborn rodents has served as a model for bronchopulmonary dysplasia (BPD) phenotypes found in a sub-population of human premature infants. We previously demonstrated that Nrf2 modulates molecular events during saccular-to-alveolar lung maturation and also has a protective role in the pathogenesis of hyperoxia-induced acute lung injury, mortality, arrest of saccular-to-alveolar transition, and lung injury, using Nrf2-deficient and wild-type neonate mice. In this review, we describe how whole-genome transcriptome analyses can identify the means through which Nrf2 transcriptionally modulates organ injury and morphology, cellular growth/proliferation, vasculature development, and immune response during BPD-like pathogenesis. We illustrate how recently developed bioinformatics tools can be used to identify sets of Nrf2-dependently modulated genes in the BPD model, and elucidate direct Nrf2 downstream targets and chemicals/drugs that may act on them. These approaches will provide significant insights into promising therapeutic agents for Nrf2-dependent treatments of complications of preterm birth like BPD.

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Close teamwork between Nrf2 and peroxiredoxins 1 and 6 for the regulation of prostaglandin D2 and E2 production in macrophages in acute inflammation

Cited by 38 publications

References 108 publications

Inflammatory Signaling and Brown Fat Activity

Inflammatory Signaling and Brown Fat Activity

Glutathionylation: a regulatory role of glutathione in physiological processes

Potential therapeutic targets in Nrf2-dependent protection against neonatal respiratory distress disease predicted by cDNA microarray analysis and bioinformatics tools

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