Nox4 promotes endothelial differentiation through chromatin remodeling

Hahner, Fabian; Moll, Franziska; Warwick, Timothy; Hebchen, D.M.; Buchmann, Giulia; Epah, Jeremy; Abplanalp, Wesley; Schader, Tim; Günther, Stefan; Gilsbach, Ralf; Brandes, Ralf P.; Schröder, Katrin

doi:10.1016/j.redox.2022.102381

Cited by 8 publications

(4 citation statements)

References 62 publications

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“…Thus, NOX4 regulates Serum Responsive Factor (SRF) protein levels and myocardin related transcription factor A (MRTFA) phosphorylation [ 33 , 34 ] – two important transcriptional regulators of smooth muscle differentiation [ 35 , 36 ]. Interestingly, a recent study linked NOX4-derived hydrogen peroxide to endothelial cell differentiation through NOX4-dependent nuclear translocation of the histone demethylase Jumonji domain-containing protein-3 (JmjD3) [ 37 ]. In other instances, the molecular mechanism by which hydrogen peroxide regulates the nucleocytoplasmic shuttling of proteins has been ascribed to the redox regulated binding of the karyopherin CRM1 with its cargo protein [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Regulation of DNA damage and transcriptional output in the vasculature through a cytoglobin-HMGB2 axis

Mathai,

Jourd'heuil,

Pham

et al. 2023

Redox Biology

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Section: Discussionmentioning

confidence: 99%

Regulation of DNA damage and transcriptional output in the vasculature through a cytoglobin-HMGB2 axis

Mathai,

Jourd'heuil,

Pham

et al. 2023

Redox Biology

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“…Histone demethylase JMJD3 mediates multiple physiological and pathological processes, including cell differentiation, proliferation, autophagy, apoptosis and proinflammatory role 38,39 . According to reports, JMJD3 is regulated by JAK/STAT, NF-κB and TGF-β/SMAD signals [40][41][42] .…”

Section: Discussionmentioning

confidence: 99%

Emodin inhibits bladder inflammation and fibrosis in mice with interstitial cystitis by regulating JMJD3

Lai,

Liu,

et al. 2023

Acta Cir. Bras.

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Interstitial cystitis/bladder pain syndrome (IC/BPS) is a devastating urological chronic pelvic pain condition. In search of a potential treatment, we investigated the effect of emodin on IC/BPS inflammation and fibrosis, and explore the potential mechanism. Methods: An experimental model of interstitial cystitis was induced by cyclophosphamide, and human bladder smooth muscle cells were treated with lipopolysaccharide to establish the cell model in vitro. In both models, inflammation-and fibrosis-related indexes were measured after emodin administration. Furthermore, the specific antagonists were used to dig for the mechanisms underlying the response to emodin treatment. Results: Emodin significantly ameliorated management of cystitis, reduced the amount of inflammatory cytokines (tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukin-1β, interleukin-8, and interleukin-6) in models, as well as reducing the synthesis of fibrosis marker including collagen1, collagen3, vimentin, fibronectin and α-smooth muscle actin. Further mechanism studies demonstrated that emodin inhibited inflammatory reaction and fibrosis through blocking lysine-specific demethylase 6B (JMJD3) expression via JAK/STAT, NF-κB and TGF-β/SMAD pathways. Conclusion: Our study reveals the critical role of emodin-JMJD3 signaling in interstitial cystitis by regulating inflammation, fibrosis, and extracellular matrix deposition in cells and tissues, and these findings provide an avenue for effective treatment of patients with cystitis.

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“…For example, the NuRD chromatin remodeling complex enzyme CHD4 is known to inhibit transcription of hypoxia-induced endothelial Ripk3, thus preventing vascular rupture [ 104 ]. Endothelial differentiation is affected by chromatin remodeling factor Nox4 [ 105 ]. Angiogenic factor receptor VEGFR is regulated in breast cancer cells by its interaction with the SWI/SNF chromatin remodeling complex [ 106 ].…”

Section: Components Of the Tme In The Light Of Chromatin Remodelingmentioning

confidence: 99%

Molecular Crosstalk between Chromatin Remodeling and Tumor Microenvironment in Multiple Myeloma

Chakraborty

Mukherjee

2022

Current Oncology

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Multiple myeloma (MM) is a complex disease driven by numerous genetic and epigenetic alterations that are acquired over time. Despite recent progress in the understanding of MM pathobiology and the availability of innovative drugs, which have pronounced clinical outcome, this malignancy eventually progresses to a drug-resistant lethal stage and, thus, novel therapeutic drugs/models always play an important role in effective management of MM. Modulation of tumor microenvironment is one of the hallmarks of cancer biology, including MM, which affects the myeloma genomic architecture and disease progression subtly through chromatin modifications. The bone marrow niche has a prime role in progression, survival, and drug resistance of multiple myeloma cells. Therefore, it is important to develop means for targeting the ecosystem between multiple myeloma bone marrow microenvironment and chromatin remodeling. Extensive gene expression profile analysis has indeed provided the framework for new risk stratification of MM patients and identifying novel molecular targets and therapeutics. However, key tumor microenvironment factors/immune cells and their interactions with chromatin remodeling complex proteins that drive MM cell growth and progression remain grossly undefined.

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Nox4 promotes endothelial differentiation through chromatin remodeling

Cited by 8 publications

References 62 publications

Regulation of DNA damage and transcriptional output in the vasculature through a cytoglobin-HMGB2 axis

Regulation of DNA damage and transcriptional output in the vasculature through a cytoglobin-HMGB2 axis

Emodin inhibits bladder inflammation and fibrosis in mice with interstitial cystitis by regulating JMJD3

Molecular Crosstalk between Chromatin Remodeling and Tumor Microenvironment in Multiple Myeloma

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