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 15 publications

(9 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

Section: Se In Adipogenesis and Adipocyte Signaling Pathwaysmentioning

confidence: 99%

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In particular, disturbance stem cell redox homeostasis by excessive production of reactive oxygen species (ROS) could lead to oxidative stress, resulting in stem cell dysfunctions such as stem cell senescence and lost stemness during long-term in vitro expansion [14, 17]. Moreover, it has been shown that ADSCs also undergo accumulation of ROS in large scale in vitro expansion [18], and precise regulation of ROS is crucial for cellular homeostasis of ADSCs [19]. Under physiological conditions, stem cells maintain low levels of ROS to preserve their stemness and to remain quiescent in mammals [14, 15, 20].…”

Section: Introductionmentioning

confidence: 99%

Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion

et al. 2019

View full text Add to dashboard Cite

Background Adipose tissue-derived mesenchymal stem cells (ADSCs) are promising candidates for regenerative medicine. However, long-term in vitro passaging leads to stemness loss and cell senescence of ADSCs, resulting in failure of ADSC-based therapy. Methods In this study, ADSCs were treated with low dose of antioxidants (reduced glutathione and melatonin) with anti-aging and stem cell protection properties in the in vitro passaging, and the cell functions including stem cell senescence, cell migration, cell multidirectional differentiation potential, and ROS content were carefully analyzed. Results We found that GSH and melatonin could maintain ADSC cell functions through reducing cell senescence and promoting cell migration, as well as by preserving stemness and multidirectional differentiation potential, through inhibiting ROS generation during long-term expansion of ADSCs. Conclusions Our results suggested that antioxidant treatment could efficiently prevent the dysfunction and preserve cell functions of ADSCs after long-term passaging, providing a practical strategy to facilitate ADSC-based therapy.

show abstract

“…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

View full text Add to dashboard Cite

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.

show abstract

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

Cited by 15 publications

References 32 publications

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

Selenium and Selenoproteins in Adipose Tissue Physiology and Obesity

Antioxidants inhibit cell senescence and preserve stemness of adipose tissue-derived stem cells by reducing ROS generation during long-term in vitro expansion

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

Contact Info

Product

Resources

About