Antioxidant effects of selenocysteine on replicative senescence in human adipose-derived mesenchymal stem cells

Suh, Nayoung; Lee, Eun-bi

doi:10.5483/bmbrep.2017.50.11.174

Cited by 14 publications

(8 citation statements)

References 32 publications

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“…Treatment with physiological doses of selenocysteine (50 and 100 nM) of adipose tissue-derived mesenchymal stem cells significantly increased cell survival and down-regulated prooxidant and proinflammatory pathways, thus possessing a protective effect on replicative senescence of adipose tissue-derived mesenchymal stem cells. These effects were accompanied by differential selenoprotein response characterized by up-regulation of GPX1 and reduced SELENOO and MSRB1 expressions [112].…”

Section: Se In Adipogenesis and Adipocyte Signaling Pathwaysmentioning

confidence: 99%

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

et al. 2020

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Selenium (Se) homeostasis is tightly related to carbohydrate and lipid metabolism, but its possible roles in obesity development and in adipocyte metabolism are unclear. The objective of the present study is to review the current data on Se status in obesity and to discuss the interference between Se and selenoprotein metabolism in adipocyte physiology and obesity pathogenesis. The overview and meta-analysis of the studies on blood Se and selenoprotein P (SELENOP) levels, as well as glutathione peroxidase (GPX) activity in obese subjects, have yielded heterogenous and even conflicting results. Laboratory studies demonstrate that Se may modulate preadipocyte proliferation and adipogenic differentiation, and also interfere with insulin signaling, and regulate lipolysis. Knockout models have demonstrated that the selenoprotein machinery, including endoplasmic reticulum-resident selenoproteins together with GPXs and thioredoxin reductases (TXNRDs), are tightly related to adipocyte development and functioning. In conclusion, Se and selenoproteins appear to play an essential role in adipose tissue physiology, although human data are inconsistent. Taken together, these findings do not support the utility of Se supplementation to prevent or alleviate obesity in humans. Further human and laboratory studies are required to elucidate associations between Se metabolism and obesity.

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Section: Se In Adipogenesis and Adipocyte Signaling Pathwaysmentioning

confidence: 99%

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

et al. 2020

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“…The therapeutic implications of SOD3 in various skin diseases such as psoriasis and atopic dermatitis have been well-studied. It has previously been shown that treatment with antioxidants can enhance the survival and therapeutic efficacy of MSCs ( 20 , 21 , 22 ). Similarly, MSCs were found to promote cerebellar neuronal survival through the secretion of SOD3 ( 23 ).…”

Section: Introductionmentioning

confidence: 99%

Superoxide dismutase 3 protects mesenchymal stem cells through enhanced autophagy and regulation of FoxO3a trafficking

2018

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Therapeutic applications of mesenchymal stem cells (MSCs) are limited due to their early death within the first few days of transplantation. Therefore, to improve the efficacy of cell-based therapies, it is necessary to manipulate MSCs so that they can resist various stresses imposed by the microenvironment. Moreover, the role of superoxide dismutase 3 (SOD3) in regulating such survival under different stress conditions remain elusive. In this study, we overexpressed SOD3 in MSCs (SOD3-MSCs) and evaluated its effect under serum starvation conditions. Nutritional limitation can decrease the survival rate of transplanted MSCs and thus can reduce their efficacy during therapy. Interestingly, we found that SOD3-MSCs exhibited reduced reactive oxygen species levels and greater survival rates than normal MSCs under serum-deprived conditions. In addition, overexpression of SOD3 attenuated starvation-induced apoptosis with increased autophagy in MSCs. Moreover, we have demonstrated that SOD3 protects MSCs against the negative effects of serum deprivation via modulation of AMP-activated protein kinase/sirtulin 1, extracellular signal-regulated kinase activation, and promoted Forkhead box O3a trafficking to the nucleus. Taken together, these results demonstrate that SOD3 promotes MSCs survival and add further evidence to the concept that SOD3-MSCs may be a potential therapeutic agent with better outcomes than normal MSCs for various diseases involving oxidative stress and compromised MSCs survival during therapy.

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“…Several antioxidants have been reported to be associated with inhibition of cellular senescence [29,30,31]. To examine whether histochrome affects cellular senescence, we investigated the long-term effect of histochrome treatment on an in vitro culture of hCPCs.…”

Section: Resultsmentioning

confidence: 99%

Therapeutic Cell Protective Role of Histochrome under Oxidative Stress in Human Cardiac Progenitor Cells

et al. 2019

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Cardiac progenitor cells (CPCs) are resident stem cells present in a small portion of ischemic hearts and function in repairing the damaged heart tissue. Intense oxidative stress impairs cell metabolism thereby decreasing cell viability. Protecting CPCs from undergoing cellular apoptosis during oxidative stress is crucial in optimizing CPC-based therapy. Histochrome (sodium salt of echinochrome A—a common sea urchin pigment) is an antioxidant drug that has been clinically used as a pharmacologic agent for ischemia/reperfusion injury in Russia. However, the mechanistic effect of histochrome on CPCs has never been reported. We investigated the protective effect of histochrome pretreatment on human CPCs (hCPCs) against hydrogen peroxide (H2O2)-induced oxidative stress. Annexin V/7-aminoactinomycin D (7-AAD) assay revealed that histochrome-treated CPCs showed significant protective effects against H2O2-induced cell death. The anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-xL were significantly upregulated, whereas the pro-apoptotic proteins BCL2-associated X (Bax), H2O2-induced cleaved caspase-3, and the DNA damage marker, phosphorylated histone (γH2A.X) foci, were significantly downregulated upon histochrome treatment of hCPCs in vitro. Further, prolonged incubation with histochrome alleviated the replicative cellular senescence of hCPCs. In conclusion, we report the protective effect of histochrome against oxidative stress and present the use of a potent and bio-safe cell priming agent as a potential therapeutic strategy in patient-derived hCPCs to treat heart disease.

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Antioxidant effects of selenocysteine on replicative senescence in human adipose-derived mesenchymal stem cells

Cited by 14 publications

References 32 publications

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

Superoxide dismutase 3 protects mesenchymal stem cells through enhanced autophagy and regulation of FoxO3a trafficking

Therapeutic Cell Protective Role of Histochrome under Oxidative Stress in Human Cardiac Progenitor Cells

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