Redox Control of Protein Arginine Methyltransferase 1 (PRMT1) Activity

Morales, Yalemi; Nitzel, Damon V.; Price, Owen M.; Gui, Shanying; Li, Jun; Qu, Jun; Hevel, Joan M.

doi:10.1074/jbc.m115.651380

Cited by 41 publications

(35 citation statements)

References 54 publications

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“…ADRBK2 is related to G-proteincoupled receptors and osphorylates the agonist-occupied form of β-adrenergic. Increased PRMT1 expression necessarily results in the increasing ADMA synthesis and demonstrates the regulated enzymatic activity in a redox-sensitive manner (Morales et al 2015). ATG4B is an autophagy-related gene which triggers autophagy by oxidizing a critical cysteine residue (He et al 2013).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Lin

Yang

Asweto

et al. 2017

Environ Sci Pollut Res

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Air pollution has been a major environment-related health threat. Most of the studies on PM toxicity have verified on the cardiovascular system and endothelial cells. However, researches on PM-induced myocardial-related toxicity are limited. This study aims to fully understand the toxic effects of PM on human myocardial cell (AC16) and explore its molecular mechanism based on microarray analysis and bioinformatics analysis. Microarray data analysis manifested that PM-induced toxicity affected expression of 472 genes compared with the control group, including 166 upregulated genes and 306 downregulated genes in human myocardial (AC16) cells. GO analysis showed that cellular processes such as immune response, cell maturation, embryonic heart tube morphogenesis, cellular response to electrical stimulus, skeletal muscle tissue regeneration, and negative regulation of signal transduction were upregulated, while regulation of transcription (DNA-dependent), rhythmic process, protein destabilization apoptotic process, and innate immune response were downregulated. The pathway analysis indicates that cell signaling pathways such as cytokine-cytokine receptor interaction, NF-κB signaling pathway, chemokine signaling pathway, endocrine and other factor-regulated calcium reabsorption, HTLV-I infection, and cell adhesion molecules (CAMs) were upregulated, while the TGF-β signaling pathway was downregulated. In addition, Signal-net showed that the TUBA4A, ADRBK2, BRIX1, SMC4, EIF5B, PRMT1, ATG4B, and NDC80 genes were significantly decreased, while the expression of the KRT6B gene was markedly increased compared with the control group. All the genes were verified by qRT-PCR. This study had provided new bioinformatics evidences in PM-induced myocardial tissue toxicity which is necessary for further cardiovascular system toxicity studies.

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Section: Discussionmentioning

confidence: 99%

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Lin

Yang

Asweto

et al. 2017

Environ Sci Pollut Res

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“…PRMT1 is regulated by alternative splicing resulting in seven different isoforms, suggesting that each isoform with its distinctive N terminus has unique substrate preference (Goulet et al, 2007). PRMT1 is regulated by oxidation (Morales et al, 2015) and microRNAs including miR503 (Li et al, 2015a). PRMT2 has been shown to function as a transcriptional repressor (Ganesh et al, 2006).…”

Section: Protein Arginine Methyltransferases Overview: Prmt Activity mentioning

confidence: 99%

Arginine Methylation: The Coming of Age

2017

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Arginine methylation is a common post-translational modification functioning as an epigenetic regulator of transcription and playing key roles in pre-mRNA splicing, DNA damage signaling, mRNA translation, cell signaling, and cell fate decision. Recently, a wealth of studies using transgenic mouse models and selective PRMT inhibitors helped define physiological roles for protein arginine methyltransferases (PRMTs) linking them to diseases such as cancer and metabolic, neurodegenerative, and muscular disorders. This review describes the recent molecular advances that have been uncovered in normal and diseased mammalian cells.

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“…Furthermore, H 2 O 2 has been shown to oxidize cysteine residues in several PRMT proteins to sulfenic acid, thus decreasing PRMT activity and histone arginine methylation (Morales et al , ). On the other hand, arsenite‐induced ROS promoted nuclear accumulation of PRMT1 and PRMT4 and methylation at H4R3 and H3R17 in the surrounding of antioxidant response elements, thus promoting binding of the transcription factor Nrf2 and antioxidant gene expression (Huang et al , ).…”

Section: Effects Of Reactive Oxygen Species On Epigenetic Mechanismsmentioning

confidence: 99%

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

Kietzmann

Petry

Shvetsova

et al. 2017

British J Pharmacology

195

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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Redox Control of Protein Arginine Methyltransferase 1 (PRMT1) Activity

Cited by 41 publications

References 54 publications

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Genome-wide transcriptional analysis of cardiovascular-related genes and pathways induced by PM2.5 in human myocardial cells

Arginine Methylation: The Coming of Age

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

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