Redox-sensitive gene-regulatory events controlling aberrant matrix metalloproteinase-1 expression

Bartling, Toni R.; Subbaram, Sita; Clark, Ryan R.; Chandrasekaran, Akshaya; Kar, Supriya; Melendez, J. Andrés

doi:10.1016/j.freeradbiomed.2014.06.017

Cited by 20 publications

(11 citation statements)

References 56 publications

(65 reference statements)

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“…ROS increased the activity of HATs in different cell types, leading to increased acetylation of H3 or H4 histones (Gilmour et al , ; Tomita et al , ; Choudhury et al , ). In support, SOD2 overexpression leading to increased H 2 O 2 levels promoted histone H3 acetylation and recruitment of the HAT p300/ CBP‐associated factor (p300/CBP) to the MMP‐1 promoter (Bartling et al , ), thus enhancing MMP‐1 expression, which has been associated with increased plaque instability in atherosclerosis (Lehrke 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

187

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: 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

187

119

View full text Add to dashboard Cite

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“…Both acute and chronic inflammatory states in vivo are associated with enhanced oxidant generation [17,28,29] and oxidative stress is considered a major factor amplifying the inflammatory state of nonhealing wound [30]. In fresh wounds, ROS release by platelets, mast cells and macrophages [31][32][33][34][35]. These changes in transcription factor activation leads to altered expression of target genes including those for inflammatory mediators and for oxidant generation (e.g.…”

Section: Oxidative Stress and Cell Signalling Pathways During Wound Hmentioning

confidence: 99%

Biocompatibility of implantable materials: An oxidative stress viewpoint

et al. 2016

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Oxidative stress occurs when the production of oxidants surpasses the antioxidant capacity in living cells. Oxidative stress is implicated in a number of pathological conditions such as cardiovascular and neurodegenerative diseases but it also has crucial roles in the regulation of cellular activities. Over the last few decades, many studies have identified significant connections between oxidative stress, inflammation and healing. In particular, increasing evidence indicates that the production of oxidants and the cellular response to oxidative stress are intricately connected to the fate of implanted biomaterials. This review article provides an overview of the major mechanisms underlying the link between oxidative stress and the biocompatibility of biomaterials. ROS, RNS and lipid peroxidation products act as chemo-attractants, signalling molecules and agents of degradation during the inflammation and healing phases. As chemo-attractants and signalling molecules, they contribute to the recruitment and activation of inflammatory and healing cells, which in turn produce more oxidants. As agents of degradation, they contribute to the maturation of the extracellular matrix at the healing site and to the degradation of the implanted material. Oxidative stress is itself influenced by the material properties, such as by their composition, their surface properties and their degradation products. Because both cells and materials produce and react with oxidants, oxidative stress may be the most direct route mediating the communication between cells and materials. Improved understanding of the oxidative stress mechanisms following biomaterial implantation may therefore help the development of new biomaterials with enhanced biocompatibility.

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“…Matrix metalloproteinase-1 (MMP-1) expression contributes to the pathogenesis of numerous degenerative diseases. MMP-1 activity is increased under oxidative stress conditions and further augmented by SOD2 overexpression due to proteasomal degradation of HDAC2 and accumulation of histone H3 acetylation marks in the MMP-1 promoter [146] . All of these redox regulatory changes were reversed by catalase overexpression.…”

Section: Impact Of Redox Signaling and Oxidative Stress On Gene Regulmentioning

confidence: 99%

Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

et al. 2015

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Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed on the emerging role of redox mechanisms regulating epigenetic pathways (e.g. miRNA, DNA methylation and histone modifications). By providing clinical correlations we discuss how oxidative stress can impact on gene regulation/activity and vise versa, how epigenetic processes, other gene regulatory mechanisms and DNA repair can influence the cellular redox state and contribute or prevent development or progression of disease.

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Redox-sensitive gene-regulatory events controlling aberrant matrix metalloproteinase-1 expression

Cited by 20 publications

References 56 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

Biocompatibility of implantable materials: An oxidative stress viewpoint

Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

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