Perfluorooctane sulfonate (PFOS) impairs the proliferation of C17.2 neural stem cells via the downregulation of GSK‐3β/β‐catenin signaling

Dong, Xuan; Jiao, Yang; Nie, Xiaobing; Xiao, Jing; Jiang, Shengyang

doi:10.1002/jat.3320

Cited by 18 publications

(5 citation statements)

References 59 publications

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“…Previous studies showed that GSK-3β played a crucial role in regulating apoptosis of NSCs, and inhibition of GSK-3β conferred NSCs resistance to apoptotic stimulator [16–18]. Additionally, it was reported that miR-26a directly targeted the 3′-UTR of GSK-3β in human adipose-derived mesenchymal stem cells [19].…”

Section: Resultsmentioning

confidence: 99%

“…It is well known that GSK-3β is a pivotal regulator of apoptosis [17]. Inhibition of GSK-3β makes NSCs more resistant to apoptotic stimulators [16–18]. Interestingly, it is reported that miR-26a could directly target the 3′-UTR of GSK-3β in human adipose-derived mesenchymal stem cells [19].…”

Section: Discussionmentioning

confidence: 99%

“…It was shown that miR-26a helped to decrease pro-apoptotic signaling in hypoxic environment [13], inhibit hypoxia-induced tubular cell apoptosis [14] and attenuate cardiac ischemia reperfusion injury [15]. Interestingly, it was reported that miR-26a directly targeted the 3′-UTR of glycogen synthase kinase 3β (GSK-3β), which plays a crucial role in apoptosis by regulating β-catenin signaling pathway in various cell types [16–18], in human adipose-derived mesenchymal stem cells [19]. However, the exact role of miR-26a in regulating NSCs apoptosis in CA-induced brain damage model remains largely unexplored.…”

Section: Introductionmentioning

confidence: 99%

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miR-26a prevents neural stem cells from apoptosis via β-catenin signaling pathway in cardiac arrest-induced brain damage

et al. 2019

Bioscience Reports

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Neural stem cells (NSCs) transplantation is one of the most promising strategies for the treatment of CA-induced brain damage. The transplanted NSCs could differentiate into new neuron and replace the damaged one. However, the poor survival of NSCs in severe hypoxic condition is the limiting step to make the best use of this kind of therapy. In the present study, we investigated whether the overexpression of miR-26a improves the survival of NSCs in hypoxic environment in vitro and in vivo. In vitro hypoxia injury model is established in NSCs by CoCl2 treatment, and in vivo cardiac arrest (CA) model is established in Sprague-Dawley (SD) rats. Quantitative real-time polymerase chain reaction is used to detect the mRNA level and Western blot is used to examine the protein level of indicated genes. TUNEL staining and flow cytometry are applied to evaluate apoptosis. Dual-luciferase reporter assay is utilized to analyze the target gene of miR-26a. The expression of miR-26a is reduced in both in vitro and in vivo hypoxic model. MiR-26a directly targets 3′-UTR of glycogen synthase kinase 3β (GSK-3β), resulting in increased β-catenin expression and decreased apoptosis of NSCs. Overexpression of miR-26a in transplanted NSCs improves the survival of NSCs and neurological function in CA rats. MiR-26a prevents NSCs from apoptosis by activating β-catenin signaling pathway in CA-induced brain damage model. Modulating miR-26a expression could be a potential strategy to attenuate brain damage induced by CA.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-26a prevents neural stem cells from apoptosis via β-catenin signaling pathway in cardiac arrest-induced brain damage

et al. 2019

Bioscience Reports

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“…All these observations suggest that BFs and PFs interact in a complex way with the cell proliferative machinery; endocrine disruptors can affect proliferation in different ways. BPA shows a significant interaction on neural stem cell proliferation and differentiation in the rat via the Wnt/β-catenin signaling pathway (Tiwari et al 2015), while PFOS disturbs cell proliferation by activating the glycogen synthase kinase-3β with resultant downregulation of cellular β-catenin (Dong et al 2016); Pierozan et al have recently described that PFOS and PFOA deregulate cyclin D1, CDK6, p21, p53, p27, ERK 1/2, and p38 in breast epithelial cells and that the cell cycle alteration persists in unexposed daughter cells after one and two passages (Pierozan et al 2020); however, the EDs doses utilized in this study were above the normal range of exposure (10-μM PFOS and 100-μM PFOA), and the overall mechanisms through which BPs and PFs at lower concentration (similar to the current daily exposure of humans) may alter regulatory cell cycle proteins need to be clarified.…”

Section: Discussionmentioning

confidence: 99%

Antenatal Exposure to Plastic Pollutants: Study of the Bisphenols and Perfluoroalkyls Effects on Human Stem Cell Models

et al. 2023

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Endocrine disruptors (EDs), such as Bisphenols (BPs) and Perfluoroalkyls (PFs), are a class of plastic pollutants widely used in industrial applications. Human exposure to these molecules usually occurs through ingestion of contaminated food and water. Once entered the human body they can interfere with endogenous hormone signaling, leading to a wide spectrum of diseases. It has been reported that BPs and PFs can cross the placental barrier accumulating in the fetal serum, but the detrimental consequences for human development remain to be clarified. Here we analyze the effects of different doses of bisphenol A and S (BPA, BPS) perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) on proliferation and mitochondrial health on different types of stem cells: through an integrated approach that combines data from pluripotent stem cells (hiPSCs) with that from the “environment” in which the embryo develops (fetal annexes-derived perinatal stem cells) we verified the potential developmental toxicity of the in utero EDs exposure. Data obtained showed that overall, BPs, and PFs tended to increase the proliferation rate of perinatal stem cells; a similar response was observed in hiPSCs exposed to very low doses of BPs and PFs, while at higher concentrations these chemicals were toxic; in addition, both the BPs and the PFs exerted a mitotoxic effects hiPSCs at all the concentration studied. All these data suggest that antenatal exposure to BPs and PFs, also at very low concentrations, may modify the biological characteristics of stem cells present in both the developing fetus and the fetal annexes, thus perturbing normal human development.

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“…One idea suggests that neurotransmitters bind to receptors in the dominant neuron or cell membrane to complete the information transfer, which leads to increased excitability and neurotoxicity (Hallgren et al, 2015;Ishida et al, 2017). Another idea suggests that PFOS might cause neurotoxicity by affecting syn-aptic plasticity (Pinkas et al, 2010;Dong et al, 2016). Moreover, both in vivo and in vitro studies have reported apoptosis of neuronal cells induced by PFOS (Chen et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Effects of perfluorooctane sulfonate (PFOS) on cognitive behavior and autophagy of male mice

Zhou,

Wang,

et al. 2023

J. Toxicol. Sci.

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Perfluorooctane sulfonate (PFOS), an emerging environmental pollutant, is reported to cause neurotoxicity in animals and humans, but its underlying mechanisms are still unclear. We used in vivo models to investigate the effects of PFOS on cognition-related behaviors and related mechanisms. After 45 days of intragastric administration of PFOS (2 mg/kg or 8 mg/kg) in 7-week-old C57BL/6 mice, muscle strength, cognitive function and anxiety-like behavior were evaluated by a series of behavioral tests. The underling mechanisms of PFOS on impaired behaviors were evaluated by HE/Nissl staining, electron microscopy observation and western blot analysis. The results indicated that PFOS-exposed mice exhibited significant cognitive impairment, anxiety, neuronal degeneration and the abnormities of synaptic ultrastructure in the cortex and hippocampus. Western blot analysis indicated that PFOS exposure increased microtubule-associated protein light chain 3 (LC3) and decreased p62 protein levels, which may be associated with activation of autophagy leading to neuron damage. In summary, our results suggest that chronic exposure to PFOS adversely affects cognitive-related behavior in mice. These findings provide new mechanistic insights into PFOS-induced neurotoxicity.

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Perfluorooctane sulfonate (PFOS) impairs the proliferation of C17.2 neural stem cells via the downregulation of GSK‐3β/β‐catenin signaling

Cited by 18 publications

References 59 publications

miR-26a prevents neural stem cells from apoptosis via β-catenin signaling pathway in cardiac arrest-induced brain damage

miR-26a prevents neural stem cells from apoptosis via β-catenin signaling pathway in cardiac arrest-induced brain damage

Antenatal Exposure to Plastic Pollutants: Study of the Bisphenols and Perfluoroalkyls Effects on Human Stem Cell Models

Effects of perfluorooctane sulfonate (PFOS) on cognitive behavior and autophagy of male mice

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