The Concise Guide to PHARMACOLOGY 2015/16: Nuclear hormone receptors

Alexander, Stephen P.H.; Cidlowski, John A.; Kelly, Eamonn; Marrion, Neil V.; Peters, John A.; Benson, Helen E.; Faccenda, Elena; Pawson, Adam J.; Sharman, Joanna L.; Southan, Christopher; Davies, Jamie A.

doi:10.1111/bph.13352

Cited by 119 publications

(41 citation statements)

References 13 publications

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“…Key protein targets and ligands in this article are hyperlinked to corresponding entries in http://www.guidetopharmacology.org, the common portal for data from the IUPHAR/BPS Guide to PHARMACOLOGY (Southan et al , ), and are permanently archived in the Concise Guide to PHARMACOLOGY 2015/16 (Alexander et al , ,b,c).…”

Section: Resultsmentioning

confidence: 99%

The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

Kietzmann

Petry

Shvetsova

et al. 2017

British J Pharmacology

189

119

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*Authors contributed equally.Cardiovascular diseases are among the leading causes of death worldwide. Reactive oxygen species (ROS) can act as damaging molecules but also represent central hubs in cellular signalling networks. Increasing evidence indicates that ROS play an important role in the pathogenesis of cardiovascular diseases, although the underlying mechanisms and consequences of pathophysiologically elevated ROS in the cardiovascular system are still not completely resolved. More recently, alterations of the epigenetic landscape, which can affect DNA methylation, post-translational histone modifications, ATP-dependent alterations to chromatin and non-coding RNA transcripts, have been considered to be of increasing importance in the pathogenesis of cardiovascular diseases. While it has long been accepted that epigenetic changes are imprinted during development or even inherited and are not changed after reaching the lineage-specific expression profile, it becomes more and more clear that epigenetic modifications are highly dynamic. Thus, they might provide an important link between the actions of ROS and cardiovascular diseases. This review will provide an overview of the role of ROS in modulating the epigenetic landscape in the context of the cardiovascular system. This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc Abbreviations 5hmC, 5-hydroxymethylcytosine; 5mC, 5-methylcytosine; 8-oxodG, 8-oxo-2 0 -deoxyguanosine; BAF, Brg1-associated factors; BER, base excision repair; BRG1, Brahma-related gene 1; BRM, Brahma; CBP, CREB binding protein; CHD, chromodomain helicase DNA-binding; CK2, casein kinase 2; CpG, 5-C-phosphate-G-3 0 ; Cys, cysteine; DNMT, DNA methyltransferase; DPF3a, double plant homeodomain (PHD) finger protein 3a; E2F1, E2F transcription factor 1; ETC, electron transport chain; EZH2, enhancer of zeste 2 PRC2 subunit; GCN5, general control nonderepressible 5; GPX1, glutathione peroxidase; HAT, histone acetyltransferases; HDAC, histone deacetylase; HDM, histone demethylase; HIF1, hypoxia-inducible factor 1; HMT, histone methyltransferases; ISWI, imitation switch; KDM, histone demethylase; LINE-1, long interspersed nuclear element-1; lncRNA, long non-coding RNA; LSD1, lysine demethylase 1A; miRNA, microRNA; mtDNA, mitochondrial DNA; nDNA, nuclear DNA; NOX, NADPH oxidases; OGG1, 8-oxoguanine DNA glycosylase; OXPHOS, oxidative phosphorylation; PARP, poly(ADP-ribose)-polymerase; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PHD, prolyl hydroxylase; PolG, polymerase γ; PPARγ, peroxisome proliferator-activated receptor gamma; PRC, polycomb repressive complex; PRMT, protein arginine N-methyltransferase; ROS, reactive oxygen species; SAM, S-adenosyl methionine; SET, Su(var)3-9, Enhancer of Zeste, Trithorax; SIRT, sirtuin; SMYD1, SET and MYND domain-containing protein 1; SNF2H, sucrose nonfermentable 2 hom...

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Section: Resultsmentioning

confidence: 99%

The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

Kietzmann

Petry

Shvetsova

et al. 2017

British J Pharmacology

189

119

View full text Add to dashboard Cite

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“…We have examined in detail the effects of tamoxifen, which, in addition to being a selective modulator of estrogen receptors (Alexander et al, 2015a), is also a potent, brain-penetrant inhibitor of PKC (O'Brian et al, 1985;Saraiva et al, 2003;de Medina et al, 2004). We have compared the effect of tamoxifen on opioid-induced tolerance to respiratory depression with that of calphostin C, another brain-penetrant drug that inhibits both conventional and novel isoforms of PKC (Kobayashi et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Effect of Tamoxifen and Brain-Penetrant Protein Kinase C and c-Jun N-Terminal Kinase Inhibitors on Tolerance to Opioid-Induced Respiratory Depression in Mice

Withey

Hill²,

Lyndon

et al. 2017

J Pharmacol Exp Ther

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Respiratory depression is the major cause of death in opioid overdose. We have previously shown that prolonged treatment of mice with morphine induces profound tolerance to the respiratory-depressant effects of the drug (Hill et al., 2016). The aim of the present study was to investigate whether tolerance to opioid-induced respiratory depression is mediated by protein kinase C (PKC) and/or c-Jun N-terminal kinase (JNK). We found that although mice treated for up to 6 days with morphine developed tolerance, as measured by the reduced responsiveness to an acute challenge dose of morphine, administration of the brain-penetrant PKC inhibitors tamoxifen and calphostin C restored the ability of acute morphine to produce respiratory depression in morphine-treated mice. Importantly, reversal of opioid tolerance was dependent on the nature of the opioid ligand used to induce tolerance, as these PKC inhibitors did not reverse tolerance induced by prolonged treatment of mice with methadone nor did they reverse the protection to acute morphineinduced respiratory depression afforded by prolonged treatment with buprenorphine. We found no evidence for the involvement of JNK in morphine-induced tolerance to respiratory depression. These results indicate that PKC represents a major mechanism underlying morphine tolerance, that the mechanism of opioid tolerance to respiratory depression is ligand-dependent, and that coadministration of drugs with PKC-inhibitory activity and morphine (as well as heroin, largely metabolized to morphine in the body) may render individuals more susceptible to overdose death by reversing tolerance to the effects of morphine.

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“…PPAR represent a family of nuclear hormone receptors consisting of 3 isoforms (α, δ, and γ [39]), and they are expressed in many organs including the ovaries, uterus, and prostate [40-42]. Numerous functions have been attributed to these receptors including the regulation of metabolism and energy homeostasis, cell proliferation, and inflammation [43-45].…”

Section: Cannabinoids and The Endocannabinoid Systemmentioning

confidence: 99%

Cannabinoids in Gynecological Diseases

Luschnig

Schicho

2019

Med Cannabis Cannabinoids

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The endocannabinoid system (ECS) is a multifunctional homeostatic system involved in many physiological and pathological conditions. The ligands of the ECS are the endocannabinoids, whose actions are mimicked by exogenous cannabinoids, such as phytocannabinoids and synthetic cannabinoids. Responses to the ligands of the ECS are mediated by numerous receptors like the classical cannabinoid receptors (CB1 and CB2) as well as ECS-related receptors, e.g., G protein-coupled receptors 18 and 55 (GPR18 and GPR55), transient receptor potential ion channels, and nuclear peroxisome proliferator-activated receptors. The ECS regulates almost all levels of female reproduction, starting with oocyte production through to parturition. Dysregulation of the ECS is associated with the development of gynecological disorders from fertility disorders to cancer. Cannabinoids that act at the ECS as specific agonists or antagonists may potentially influence dysregulation and, therefore, represent new therapeutic options for the therapy of gynecological disorders.

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The Concise Guide to PHARMACOLOGY 2015/16: Nuclear hormone receptors

Cited by 119 publications

References 13 publications

The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

Effect of Tamoxifen and Brain-Penetrant Protein Kinase C and c-Jun N-Terminal Kinase Inhibitors on Tolerance to Opioid-Induced Respiratory Depression in Mice

Cannabinoids in Gynecological Diseases

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