ArticleOxidative medicine and cellular longevity2013
Inhibition of nuclear Nox4 activity by plumbagin: effect on proliferative capacity in human amniotic stem cells.
Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Gene network analysis combined with preclinical studies to identify and elucidate the mechanism of action of novel irreversible Keap1 inhibitor for Parkinson's disease.Molecular diversity · 2025Article
- Plumbagin, a Natural Compound with Several Biological Effects and Anti-Inflammatory Properties.Life (Basel, Switzerland) · 2023Review
- Plumbagin protects H9c2 cardiomyocytes against TBHP-induced cytotoxicity by alleviating ROS-induced apoptosis and modulating autophagy.Experimental and therapeutic medicine · 2022Article
- Exosomes Derived from Human Amniotic Fluid Mesenchymal Stem Cells Preserve Microglia and Neuron Cells from Aβ.International journal of molecular sciences · 2022Article
- Article
- The Interplay between HGF/c-met Axis and Nox4 in BRAF Mutated Melanoma.International journal of molecular sciences · 2021Article
- Oxidative Stress in Alzheimer's Disease:Oxidative medicine and cellular longevity · 2020Article
- Nuclear Nox4 interaction with prelamin A is associated with nuclear redox control of stem cell aging.Aging · 2018Article
- NADPH oxidase 4 regulates anoikis resistance of gastric cancer cells through the generation of reactive oxygen species and the induction of EGFR.Cell death & disease · 2018Article
- Sulforaphane Modulates AQP8-Linked Redox Signalling in Leukemia Cells.Oxidative medicine and cellular longevity · 2018Article
- Nuclear membrane-localised NOX4D generates pro-survival ROS in FLT3-ITD-expressing AML.Oncotarget · 2017Article
- Plumbagin Protects Mice from Lethal Sepsis by Modulating Immunometabolism Upstream of PKM2.Molecular medicine (Cambridge, Mass.) · 2016Article
- Luminal flow induces NADPH oxidase 4 translocation to the nuclei of thick ascending limbs.Physiological reports · 2016Article
- Reversal of the glycolytic phenotype of primary effusion lymphoma cells by combined targeting of cellular metabolism and PI3K/Akt/ mTOR signaling.Oncotarget · 2016Article
- Role of hepatocyte growth factor in the immunomodulation potential of amniotic fluid stem cells.Stem cells translational medicine · 2015Article
- Nuclear Nox4 Role in Stemness Power of Human Amniotic Fluid Stem Cells.Oxidative medicine and cellular longevity · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human amniotic fluid stem cells (AFSC) with multilineage differentiation potential are novel source for cell therapy. However, in vitro expansion leads to senescence affecting differentiation and proliferative capacities. Reactive oxygen species (ROS) have been involved in the regulation of stem cell pluripotency, proliferation, and differentiation. Redox-regulated signal transduction is coordinated by spatially controlled production of ROS within subcellular compartments. NAD(P)H oxidase family, in particular Nox4, has been known to produce ROS in the nucleus; however, the mechanisms and the meaning of this function remain largely unknown. In the present study, we show that Nox4 nuclear expression (nNox4) increases during culture passages up to cell cycle arrest and the serum starvation causes the same effect. With the decrease of Nox4 activity, obtained with plumbagin, a decline of nuclear ROS production and of DNA damage occurs. Moreover, plumbagin exposure reduces the binding between nNox4 and nucleoskeleton components, as Matrin 3. The same effect was observed also for the binding with phospho-ERK, although nuclear ERK and P-ERK are unchanged. Taken together, we suggest that nNox4 regulation may have important pathophysiologic effects in stem cell proliferation through modulation of nuclear signaling and DNA damage.
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