Nox2 and Nox4 regulate self-renewal of murine induced-pluripotent stem cells

Kang, Xueling; Wei, Xiangxiang; Jiang, Li; Niu, Cong; Zhang, Jianyi; Chen, SF; Meng, Dan

doi:10.1002/iub.1574

Cited by 16 publications

(21 citation statements)

References 40 publications

(62 reference statements)

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“…Targeted silencing of Nox2/4 decreases intracellular ROS levels and total number of murine iPSCs resulting in reduced expression of insulin-like growth factor-1 (IGF-1), IGF-1 receptor and phosphorylation of ERK 1/2. Furthermore, expression of the stemness genes Sox2 and Oct4 was lower in Nox2/Nox4-deficient iPSCs, and higher in Nox2/Nox4-overexpressing iPSCs suggesting that Nox2-derived ROS contributes to stem cell pluripotency maintenance and self-renewal [ 116 ].…”

Section: The Role Of Nox In Stem Cellsmentioning

confidence: 99%

Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate

et al. 2017

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The generation of reactive oxygen species (ROS) and an imbalance of antioxidant defence mechanisms can result in oxidative stress. Several pro-atherogenic stimuli that promote intimal-medial thickening (IMT) and early arteriosclerotic disease progression share oxidative stress as a common regulatory pathway dictating vascular cell fate. The major source of ROS generated within the vascular system is the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes (Nox), of which seven members have been characterized. The Nox family are critical determinants of the redox state within the vessel wall that dictate, in part the pathophysiology of several vascular phenotypes. This review highlights the putative role of ROS in controlling vascular fate by promoting endothelial dysfunction, altering vascular smooth muscle phenotype and dictating resident vascular stem cell fate, all of which contribute to intimal medial thickening and vascular disease progression.

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Section: The Role Of Nox In Stem Cellsmentioning

confidence: 99%

Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate

et al. 2017

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“…Furthermore, some studies claim that ROS have also a role either in stem cell maintenance and differentiation, or in the self-renewal capacity of the neural stem cells (Le Belle et al, 2011;Chaudhari et al, 2014;Kang et al, 2016). ROS production is physiologically highly regulated by the balance between ROS producing and antioxidant agents.…”

Section: Introductionmentioning

confidence: 99%

NOX4 regulates TGFβ-induced proliferation and self-renewal in glioblastoma stem cells

García-Gómez

Dadras²,

Bellomo³

et al. 2019

Preprint

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Glioblastoma (GBM) is the most aggressive and common glioma subtype with a median survival of 15 months after diagnosis. Current treatments have limited therapeutic efficacy, thus more effective approaches are needed. The glioblastoma tumoral mass is characterized by a small cellular subpopulation, the Glioblastoma stem cells (GSCs), which has been held accountant for initiation, invasion, proliferation, relapse and resistance to chemo-and radiotherapy. Targeted therapies against GSCs are crucial, and so is the understanding of the molecular mechanisms that govern the GSCs.Transforming growth factor β (TGFβ), platelet growth factor (PDGF) signalling and Reactive Oxygen Species (ROS) production govern and regulate cancer-stem cell biology. In this work, we focus on the role of the NADPH oxidase 4 (NOX4) downstream of TGFβ signalling in the GSCs. NOX4 utilises NADPH to generate ROS; TGFβ induces NOX4 expression, thus increasing ROS production.Interestingly, NOX4 itself regulates GSC self-renewal and modulates Since TGFβ regulates PDGFB in GSC, we analysed how PDGFB modulates NOX4 expression and increases ROS production. Both TGFβ and PDGF signalling regulate GSC proliferation in a NOX4/ROS-dependent manner. The transcription factor NRF2, involved in the transcriptional regulation of antioxidant and metabolic responses, is regulated by both TGFβ and NOX4. This results in an antioxidant response, which positively contributes to GSC self-renewal and proliferation. In conclusion, this work functionally establishes NOX4 as a key mediator of GSC biology.

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“…It is encoded on human chromosome 11. Together with Nox2, Nox4 activity is necessary for the maintenance of stemness of induced pluripotent stem cells [ 59 ]. An excellent review on this human Nox isoform was published relatively recently [ 60 ].…”

Section: Introductionmentioning

confidence: 99%

The defense and signaling role of NADPH oxidases in eukaryotic cells

Breitenbach

Rinnerthaler

Weber

et al. 2018

Wien Med Wochenschr

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SummaryThis short review article summarizes what is known clinically and biochemically about the seven human NADPH oxidases. Emphasis is put on the connection between mutations in the catalytic and regulatory subunits of Nox2, the phagocyte defense enzyme, with syndromes like chronic granulomatous disease, as well as a number of chronic inflammatory diseases. These arise paradoxically from a lack of reactive oxygen species production needed as second messengers for immune regulation. Both Nox2 and the six other human NADPH oxidases display signaling functions in addition to the functions of these enzymes in specialized biochemical reactions, for instance, synthesis of the hormone thyroxine. NADPH oxidases are also needed by Saccharomyces cerevisiae cells for the regulation of the actin cytoskeleton in times of stress or developmental changes, such as pseudohyphae formation. The article shows that in certain cancer cells Nox4 is also involved in the re-structuring of the actin cytoskeleton, which is required for cell mobility and therefore for metastasis.

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Nox2 and Nox4 regulate self-renewal of murine induced-pluripotent stem cells

Cited by 16 publications

References 40 publications

Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate

Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate

NOX4 regulates TGFβ-induced proliferation and self-renewal in glioblastoma stem cells

The defense and signaling role of NADPH oxidases in eukaryotic cells

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