The Histone Methyltransferase SETDB1 Modulates Survival of Spermatogonial Stem/Progenitor Cells Through NADPH Oxidase

Li, Xueliang; Chen, Xiaoxu; Liu, Yingdong; Zhang, Pengfei; Zheng, Yi

doi:10.3389/fgene.2020.00997

Cited by 5 publications

(3 citation statements)

References 55 publications

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“…Moreover, very recently, Liu and co-workers highlighted the involvement of NOX4 in the modulation of Spermatogonial Stem/Progenitor Cells survival mediated by Histone Methyltransferase SETDB1 [ 97 ].…”

Section: Stem Cells and Progenitor Cells: Ros And Nox Functionsmentioning

confidence: 99%

NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function

et al. 2021

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One of the major sources of reactive oxygen species (ROS) generated within stem cells is the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes (NOXs), which are critical determinants of the redox state beside antioxidant defense mechanisms. This balance is involved in another one that regulates stem cell fate: indeed, self-renewal, proliferation, and differentiation are decisive steps for stem cells during embryo development, adult tissue renovation, and cell therapy application. Ex vivo culture-expanded stem cells are being investigated for tissue repair and immune modulation, but events such as aging, senescence, and oxidative stress reduce their ex vivo proliferation, which is crucial for their clinical applications. Here, we review the role of NOX-derived ROS in stem cell biology and functions, focusing on positive and negative effects triggered by the activity of different NOX isoforms. We report recent findings on downstream molecular targets of NOX-ROS signaling that can modulate stem cell homeostasis and lineage commitment and discuss the implications in ex vivo expansion and in vivo engraftment, function, and longevity. This review highlights the role of NOX as a pivotal regulator of several stem cell populations, and we conclude that these aspects have important implications in the clinical utility of stem cells, but further studies on the effects of pharmacological modulation of NOX in human stem cells are imperative.

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Section: Stem Cells and Progenitor Cells: Ros And Nox Functionsmentioning

confidence: 99%

NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function

et al. 2021

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“…It also safeguards fatty acids from oxidation and has anti-apoptotic and anti-aging effects on cells through cell signaling and response. Melatonin is known to reduce the amount of reactive oxygen species (ROS) production in cells, thereby preventing DNA mutation caused by oxidative stress [ 6 - 8 ]. Because melatonin has both hydrophilic and lipophilic properties, it can aid in safeguarding mammalian gametes and embryos while they are being cultured.…”

Section: Introductionmentioning

confidence: 99%

The effect of biological mechanisms of melatonin on the proliferation of spermatogonial stem cells: a systematic review

Navid,

Saadatian,

Talebi

et al. 2024

Anat Cell Biol

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In the last decade, melatonin has gained recognition as a potent scavenger and an effective antioxidant capable of neutralizing free radicals, including reactive oxygen species. Additionally, it exhibits anti-apoptotic properties. In this review, we will examine a compilation of articles that explore the cellular signaling function of melatonin on spermatogonial stem cells (SSCs) and adjacent cells such as Sertoli and Leydig cells. These cells play a crucial role in the proliferation of SSCs both in vitro and in vivo . In this review, we analyze the function of melatonin in the proliferation of SSCs from other aspects. For this purpose, we examine the articles based on the presence of melatonin on SSCs in four groups: As a supplement in SSCs medium culture, SSCs three-dimensional culture system, SSCs freezing medium, and as a therapeutic factor in vivo . Mechanisms of growth and proliferation of SSCs were considered. The purpose of this study is to investigate the potential effects of melatonin as a powerful antioxidant or growth stimulant for SSCs, both in vivo and in vitro .

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“…In addition, the G9a, a H3K9 methyltransferase, was required for meiosis during spermatogenesis 16 . The effects of melatonin focused on epigenetic modifications of histones caused by the oxidative stress 17 . Nevertheless, whether PM2.5‐related male reproductive toxicity involves changes in G9a‐mediated H3K9 methylation and the possible protective functions of melatonin are still unknown.…”

Section: Introductionmentioning

confidence: 99%

Melatonin ameliorates PM2.5‐induced spermatogenesis disorder by preserving H3K9 methylation and SIRT3

Liu,

Zhao,

Dong

et al. 2023

Environmental Toxicology

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There was a link between exposure to PM2.5 and male infertility. Melatonin has beneficial effects on the male reproductive processes. How PM2.5 caused spermatogenesis disturbance and whether melatonin could prevent PM2.5‐induced reproductive toxicity have remained unclear. The results showed that PM2.5 could inhibit the Nrf2‐mediated antioxidant pathway and distinctly increase the cell apoptosis in testes. Moreover, PM2.5 also perturbed the process of meiosis by modulating meiosis‐associated proteins such as γ‐H2AX and Stra8. Mechanistically, PM2.5 inhibited G9a‐dependent H3K9 methylation and SIRT3‐mediated p53 deacetylation, which consistent with decreased sperm count and motility rate in ApoE−/− mice. Further investigation revealed melatonin effectively alleviated PM2.5‐induced meiosis inhibition by preserving H3K9 methylation. Melatonin also alleviated PM2.5‐induced apoptosis by regulating SIRT3‐mediated p53 deacetylation. Overall, our study revealed PM2.5 resulted in spermatogenesis disorder by perturbing meiosis via G9a‐dependent H3K9 di‐methylation and causing cell apoptosis via SIRT3/p53 deacetylation pathway and provided promising insights into the protective role of melatonin in air pollution associated with male infertility.

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The Histone Methyltransferase SETDB1 Modulates Survival of Spermatogonial Stem/Progenitor Cells Through NADPH Oxidase

Cited by 5 publications

References 55 publications

NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function

NADPH Oxidases: Redox Regulators of Stem Cell Fate and Function

The effect of biological mechanisms of melatonin on the proliferation of spermatogonial stem cells: a systematic review

Melatonin ameliorates PM2.5‐induced spermatogenesis disorder by preserving H3K9 methylation and SIRT3

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