Supplementation freeze-thawed media with selenium protect adipose-derived mesenchymal stem cells from freeze-thawed induced injury

Valadbeygi, Arash; Naji, Tahereh; Pirnia, Afshin; Gholami, Mohammadreza

doi:10.1016/j.cryobiol.2016.08.009

Cited by 8 publications

(3 citation statements)

References 25 publications

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“…Early documents have shown that selenium could have a protective effect on the decreased expression of death receptor pathway related molecules. 53,54 In the present study, our research revealed that the expression levels of FAS, FASL, TNFα, TNF-R1, CASPASE-3, CASPASE-8 and CASPASE-10 were significantly decreased in the AFB 1 + Se group when compared with the AFB 1 group. However, no significant differences of these values were observed between the +Se group and the control group.…”

Section: Discussionsupporting

confidence: 55%

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB₁through death receptor and endoplasmic reticulum pathways

et al. 2018

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Section: Discussionsupporting

confidence: 55%

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB₁through death receptor and endoplasmic reticulum pathways

et al. 2018

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“…This result implies that the reduction of ROS plays a pivotal role in in vitro expansion and long-term survival of MSCs. Although selenium is well known to be an effective antioxidant and free radical scavenger, only a few studies on its effects on MSCs have been recently reported and none on its effects on extending the proliferation and differentiation potential of MSCs [ 45 – 47 ]. Meanwhile, recent research has provided some interesting clues to explain the observed bFGF-induced ROS reduction.…”

Section: Discussionmentioning

confidence: 99%

Additive effect of bFGF and selenium on expansion and paracrine action of human amniotic fluid-derived mesenchymal stem cells

et al. 2018

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BackgroundMesenchymal stem cell-derived conditioned medium (MSC-CM) has emerged as a promising cell-free tool for restoring degenerative diseases and treating traumatic injuries. The present study describes the effect of selenium as a reactive oxygen species (ROS) scavenger and its additive effect with basic fibroblast growth factor (bFGF) on in vitro expansion of amniotic fluid (AF)-MSCs and the paracrine actions of AF-MSC-CM as well as the associated cellular and molecular mechanisms.MethodsIn this study, we obtained CM from human AF-MSCs cultured with selenium. The stemness of selenium-treated AF-MSCs was evaluated by cell growth and differentiation potential. Human fibroblasts were treated with AF-MSC-CM and analyzed for cell signaling changes. For in vivo wound healing assay, ICR mice with a full-thickness skin wound were used.ResultsSelenium played a critical role in in vitro expansion of AF-MSCs through activation of the AKT-ERK1/2, Smad2, and Stat3 signaling pathways along with inactivation of GSK3β. When administered together with bFGF, it showed remarkable effect in inhibiting ROS accumulation and preserving their multipotency. Proliferation and migration of human dermal fibroblasts and in vivo wound healing were improved in the CMs derived from AF-MSCs exposed to selenium and bFGF, which was caused by the Smad2, AKT-MEK1/2-ERK, and NFκB signaling triggered by the paracrine factors of AF-MSCs, such as TGF-β, VEGF, and IL-6. Our results suggest the following: (a) supplementation of selenium in AF-MSC culture contributes to in vitro expansion and preservation of multipotency, (b) ROS accumulation causes progressive losses in proliferative and differentiation potential, (c) the separate activities of bFGF and selenium in MSCs exert an additive effect when used together, and (d) the additive combination improves the therapeutic effects of AF-MSC-derived CMs on tissue repair and regeneration.ConclusionAntioxidants, such as selenium, should be considered as an essential supplement for eliciting the paracrine effects of MSC-CMs.Electronic supplementary materialThe online version of this article (10.1186/s13287-018-1058-z) contains supplementary material, which is available to authorized users.

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“…In general, our study showed an antiapoptotic effect for selenium. The antiapoptotic effect of selenium may be resulted from its antioxidant effects [ 23 ]. A controversial hypothesis is that anticancer effect of selenium is through induction of apoptosis [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of Selenium on Expression of Apoptosis-Related Genes in Cryomedia of Mice Ovary after Vitrification

Nori-Garavand

Hadipour

Narimani

et al. 2020

BioMed Research International

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Introduction. Freezing of ovarian tissue is used for preservation of fertility. The freezing-thawing process is accompanied by oxidative stress and induction of apoptosis. Apoptosis is a complex process that has been studied in animal models. The present study was aimed at investigating the effect of selenium on suppression of apoptosis during vitrification-thawing process of mice ovary via studying expression of apoptosis-related genes, and also, we aimed to design statistical models for the roles of single genes and gene-gene interactions in suppression of apoptosis. Methods. A total of 10 right ovary samples from 10 mice were randomly divided into two groups of selenium treatment (at dose 5 μg/ml sodium selenite, through adding to the media) and control group. Vitrification-thawing process was done according to the existed protocols. Real-time PCR was used for gene expression study. The apoptosis gene profile included P53, Bax, Fas, and Bcl-2. General linear model was applied to study single gene associations and gene-gene interactions. Results. From the studied genes, P53 showed a significant downregulation in the selenium group in comparison to the control group (∆∆CT=1.96; P=0.013; relative expression RE=0.28). Bcl-2 showed a significant upregulation in the selenium group in comparison to the control group (∆∆CT=−2.49; P<0.001; RE=3.49). No significant result was found for other genes. According to the multiple models, Bcl-2 showed a protective single gene association (beta=−0.33; P=0.032), and Fas∗Bcl-2 interaction was significantly positive (beta=0.19; P=0.036). Conclusion. Addition of selenium to cryomedia of vitrification-thawing process could reduce the apoptosis induced by freezing-thawing stress in mice ovary via downregulation of P53 and upregulation of Bcl-2 at transcription level. Multivariable statistical models should be performed in future researches to study biological systems.

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Supplementation freeze-thawed media with selenium protect adipose-derived mesenchymal stem cells from freeze-thawed induced injury

Cited by 8 publications

References 25 publications

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB₁through death receptor and endoplasmic reticulum pathways

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB₁through death receptor and endoplasmic reticulum pathways

Additive effect of bFGF and selenium on expansion and paracrine action of human amniotic fluid-derived mesenchymal stem cells

Effect of Selenium on Expression of Apoptosis-Related Genes in Cryomedia of Mice Ovary after Vitrification

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Supplementation freeze-thawed media with selenium protect adipose-derived mesenchymal stem cells from freeze-thawed induced injury

Cited by 8 publications

References 25 publications

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB1through death receptor and endoplasmic reticulum pathways

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB1through death receptor and endoplasmic reticulum pathways

Additive effect of bFGF and selenium on expansion and paracrine action of human amniotic fluid-derived mesenchymal stem cells

Effect of Selenium on Expression of Apoptosis-Related Genes in Cryomedia of Mice Ovary after Vitrification

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Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB₁through death receptor and endoplasmic reticulum pathways

Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFB₁through death receptor and endoplasmic reticulum pathways