NADPH Oxidase 4 Regulates Inflammation in Ischemic Heart Failure: Role of Soluble Epoxide Hydrolase

Stevenson, Mark; Canugovi, Chandrika; Vendrov, Aleksandr E.; Hayami, Takayuki; Bowles, Dawn E.; Krause, Karl-Heinz; Madamanchi, Nageswara R.; Runge, Marschall S.

doi:10.1089/ars.2018.7548

Cited by 31 publications

(26 citation statements)

References 78 publications

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“…In particular, NOX4‐derived ROS is important for the survival of many cancer types . However, recent reports have suggested that NOX4 activity perturbs redox balance in cells, resulting in cell death . These reports are consistent with our result that NOX4 inhibition finally blocked the PS exposure and DNA fragmentation of Entamoeba ‐stimulated Jurkat T cells.…”

Section: Discussionsupporting

confidence: 92%

“…In an ischaemic heart failure model, NOX4 directly increases cardiomyocyte death. Moreover, cardiomyocyte death was reduced in a NOX4 knockout mice, whereas cell death was increased by NOX4 overexpression . In addition, it has been reported that human retinal endothelial cells treated with high glucose induce NOX4‐derived ROS and eventually increase cell death .…”

Section: Discussionmentioning

confidence: 98%

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NOX4 activation is involved in ROS‐dependent Jurkat T‐cell death induced by Entamoeba histolytica

Lee

Kim

Min

et al. 2019

Parasite Immunology

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| INTRODUC TI ONEntamoeba histolytica, an enteric protozoan and tissue-invasive parasite, causes amoebic colitis and occasionally liver abscess in humans. 1 The Entamoeba cyst that enters the human body is converted to trophozoites through excystation. Trophozoites subsequently bind to host cells via amoebic Gal/GalNAc lectin and induce host cell death through apoptosis or necrosis. E histolytica induces host cell death via an elevation in intracellular Ca 2+ , ROS generation, caspase-3 activation, calpain activation, O-deGlcNAcylation and the degradation of cytoskeletal proteins. 2-5 However, the signalling molecule required for amoeba-induced host cell death has not been fully identified.Reactive oxygen species (ROS) acts as a second messenger in the cell and plays an important role in various intracellular processes, such as host defence, cell growth, differentiation and cell death. NADPH oxidases (NOX) are a major source of ROS. To date, mammalian cells are known to have a total of seven isoforms of NOX, which include NOX1-5, DUOX1 and DUOX2. It has been reported that the expression level and activity of each type of NOX differs by cell and tissue. 6 The most well-known NOX isoform, NOX2, is primarily in phagocytes and is used as a defence mechanism to kill infecting bacteria via NOX2-derived ROS. In nonphagocytic cells, other NOX isoforms (NOX1, NOX4 and NOX5) play a role in various intracellular processes. 6 NOX4 was first identified in the kidney and is present in nearly all cells. 6 NOX4 is found Abstract Aims: Entamoeba histolytica can induce host cell death through induction of various intracellular signalling pathways. The responses triggered by E. histolytica are closely associated with tissue pathogenesis and immune evasion. Although E. histolytica can induce reactive oxygen species (ROS) in host cells, which NADPH oxidase (NOX) isoform contributes to amoeba-triggered Jurkat T-cell death is unclear. In this study, we investigated the signalling role of NOX4-derived ROS in E. histolytica-induced Jurkat T-cell death process. Methods and results: In resting-state Jurkat T cells, NOX4 is strongly expressed. When Jurkat T cells were incubated with live E. histolytica trophozoites, intracellular ROS was significantly increased compared to cells incubated with medium alone. E. histolytica-induced ROS production was inhibited by pretreating Jurkat T cells with a NOX inhibitor. In addition, pretreating Jurkat T cells with a NOX inhibitor (Diphenyleneiodonium chloride) effectively blocked E. histolytica-induced phosphatidylserine (PS) exposure and DNA fragmentation of host cells. Moreover, siRNA-mediated knockdown of NOX4 protein expression in Jurkat T cells prevented E. histolytica-induced ROS generation and DNA fragmentation. Conclusion:These results suggest that NOX4 has a critical role in ROS-dependent cell death process in Jurkat T cells induced by E. histolytica. K E Y W O R D SEntamoeba histolytica, host cell death, NADPH oxidase, reactive oxygen species

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 98%

NOX4 activation is involved in ROS‐dependent Jurkat T‐cell death induced by Entamoeba histolytica

Lee

Kim

Min

et al. 2019

Parasite Immunology

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“…Importantly, the expression of sEH in ligation hearts was significantly greater than that in hearts from wild-type mice. In addition, the inflammation factors were ameliorated when treated with sEH inhibitors ( Stevenson et al, 2019 ). In another HF model induced by LPS, the cardiac function was decreased, as evaluated by hemodynamic analysis and echocardiography, while sEH deficiency attenuated LPS-induced cardiac dysfunction.…”

Section: The Role Of Eets In the Pathological Changes Of Cardiac Remomentioning

confidence: 99%

The Role of Epoxyeicosatrienoic Acids in Cardiac Remodeling

Lai

Chen

2021

Front. Physiol.

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Epoxyeicosatrienoic acids (EETs) are metabolites of arachidonic acid by cytochrome P450 (CYP) epoxygenases, which include four regioisomers: 5,6-EET, 8,9-EET, 11,12-EET, and 14,15-EET. Each of them possesses beneficial effects against inflammation, fibrosis, and apoptosis, which could combat cardiovascular diseases. Numerous studies have demonstrated that elevation of EETs by overexpression of CYP2J2, inhibition of sEH, or treatment with EET analogs showed protective effects in various cardiovascular diseases, including hypertension, myocardial infarction, and heart failure. As is known to all, cardiac remodeling is the major pathogenesis of cardiovascular diseases. This review will begin with the introduction of EETs and their protective effects in cardiovascular diseases. In the following, the roles of EETs in cardiac remodeling, with a particular emphasis on myocardial hypertrophy, apoptosis, fibrosis, inflammation, and angiogenesis, will be summarized. Finally, it is suggested that upregulation of EETs is a potential therapeutic strategy for cardiovascular diseases. The EET-related drug development against cardiac remodeling is also discussed, including the overexpression of CYP2J2, inhibition of sEH, and the analogs of EET.

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“…Stevenson et al found that CCL5 level increased significantly in the human hearts with ischemic cardiomyopathy compared to control nonfailing hearts. 32 What’s more, Montecucco et al reported that the incidence of postinfarct heart failure was significantly reduced by treatment with anti-CCL5 mAb in chronic cardiac ischaemia mouse models. 27 These findings show that CCL5 play an important role in the process of IHF and NIHF.…”

Section: Discussionmentioning

confidence: 99%

Identification of Independent and Communal Differentially Expressed Genes as Well as Potential Therapeutic Targets in Ischemic Heart Failure and Non-Ischemic Heart Failure

Wang¹,

Zhang²,

Xu³

et al. 2021

PGPM

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Background Heart failure (HF) is a rapidly growing public health problem, and its two main etiological types are non-ischemic heart failure (NIHF) and ischemic heart failure (IHF). However, the independent and common mechanisms of NIHF and IHF have not been fully elucidated. Here, bioinformatic analysis was used to characterize the difference and independent pathways for IHF and NIHF, and more importantly, to unearth the common potential markers and therapeutic targets in IHF and NIHF. Methods Two data sets with accession numbers GSE26887 and GSE84796 were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the independent and communal DEGs of NIHF and IHF, a functional annotation, protein–protein interaction (PPI) network analysis, co-expression and drug–gene interaction prediction analysis, and mRNA-miRNA regulatory network analysis were performed for DEGs. Results We found 1146 independent DEGs (DEGs2) of NIHF mainly enriched in transcription-related and 2595 independent DEGs (DEGs3) of IHF mainly enriched in immune-related. Moreover, 185 communal DEGs (DEGs1) were found between NIHF and IHF, including 93 upregulated genes and 92 downregulated genes. Pathway enrichment analysis results showed that GPCR pathways and biological processes are closely related to the occurrence of HF. In addition, three hub genes were identified from PPI network, including CCL5, C5 and TLR3. Conclusion The identification of DEGs and hub genes in this study contributes to a novel perception for potential functional mechanisms and biomarkers or therapeutic targets in NIHF and IHF.

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NADPH Oxidase 4 Regulates Inflammation in Ischemic Heart Failure: Role of Soluble Epoxide Hydrolase

Cited by 31 publications

References 78 publications

NOX4 activation is involved in ROS‐dependent Jurkat T‐cell death induced by Entamoeba histolytica

NOX4 activation is involved in ROS‐dependent Jurkat T‐cell death induced by Entamoeba histolytica

The Role of Epoxyeicosatrienoic Acids in Cardiac Remodeling

Identification of Independent and Communal Differentially Expressed Genes as Well as Potential Therapeutic Targets in Ischemic Heart Failure and Non-Ischemic Heart Failure

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