Regulation of the mitochondrial reactive oxygen species: Strategies to control mesenchymal stem cell fates ex vivo and in vivo

Hu, Chenxia; Zhao, Lingfei; Peng, Conggao; Li, Lanjuan

doi:10.1111/jcmm.13835

Cited by 54 publications

(49 citation statements)

References 139 publications

(221 reference statements)

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“…Correspondingly, mitochondria-mediated fission contributes to immature mitochondrial morphology in BMSCs (Feng et al, 2019). These mitochondrial characteristics in MSCs are consistent with the metabolic level of MSCs in which mitochondria maintain low mitochondrial activity, low ROS lever and provide energy primarily through glycolysis (Fillmore et al, 2015;Hu et al, 2018a). However, embryonic mouse neural stem cells (NSCs) have increased mitochondrial lengths and relatively developed networks compared with ESCs or iPSCs, although these cells depend on aerobic glycolytic metabolism (Khacho et al, 2016).…”

Section: Morphological Characteristics Of Mitochondria In Mscsmentioning

confidence: 63%

Mitochondrial Dynamics: Fission and Fusion in Fate Determination of Mesenchymal Stem Cells

Ren

Chen

et al. 2020

Front. Cell Dev. Biol.

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Mesenchymal stem cells (MSCs) are pivotal to tissue homeostasis, repair, and regeneration due to their potential for self-renewal, multilineage differentiation, and immune modulation. Mitochondria are highly dynamic organelles that maintain their morphology via continuous fission and fusion, also known as mitochondrial dynamics. MSCs undergo specific mitochondrial dynamics during proliferation, migration, differentiation, apoptosis, or aging. Emerging evidence suggests that mitochondrial dynamics are key contributors to stem cell fate determination. The coordination of mitochondrial fission and fusion is crucial for cellular function and stress responses, while abnormal fission and/or fusion causes MSC dysfunction. This review focuses on the role of mitochondrial dynamics in MSC commitment under physiological and stress conditions. We highlight mechanistic insights into modulating mitochondrial dynamics and mitochondrial strategies for stem cell-based regenerative medicine. These findings shed light on the contribution of mitochondrial dynamics to MSC fate and MSC-based tissue repair.

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Section: Morphological Characteristics Of Mitochondria In Mscsmentioning

confidence: 63%

Mitochondrial Dynamics: Fission and Fusion in Fate Determination of Mesenchymal Stem Cells

Ren

Chen

et al. 2020

Front. Cell Dev. Biol.

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“…We highlight the regulatory effect of cP1P on HIF1α expression and nuclear translocation for the enhancement of therapeutic potential of MSCs under hypoxia. Previous studies have reported that mitochondrial ROS is a major risk factor of apoptosis and immunopotency suppression in MSCs exposed to hypoxia 43,[45][46][47] . Aberrant control of mitochondrial ROS level impairs the integrity of mitochondrial membranes, thereby activating the caspasedependent apoptosis signaling pathway 48 .…”

Section: Discussionmentioning

confidence: 99%

O-cyclic phytosphingosine-1-phosphate stimulates HIF1α-dependent glycolytic reprogramming to enhance the therapeutic potential of mesenchymal stem cells

et al. 2019

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O-cyclic phytosphingosine-1-phosphate (cP1P) is a novel chemically synthesized sphingosine metabolite derived from phytosphingosine-1-phosphate. Although structurally similar to sphingosine-1-phosphate (S1P), its biological properties in stem cells remain to be reported. We investigated the effect of cP1P on the therapeutic potential of mesenchymal stem cells (MSCs) and their regulatory mechanism. We found that, under hypoxia, cP1P suppressed MSC mitochondrial dysfunction and apoptosis. Metabolic data revealed that cP1P stimulated glycolysis via the upregulation of glycolysis-related genes. cP1P-induced hypoxia-inducible factor 1 alpha (HIF1α) plays a key role for MSC glycolytic reprogramming and transplantation efficacy. The intracellular calcium-dependent PKCα/mammalian target of the rapamycin (mTOR) signaling pathway triggered by cP1P regulated HIF1α translation via S6K1, which is critical for HIF1 activation. Furthermore, the cP1P-activated mTOR pathway induced bicaudal D homolog 1 expression, leading to HIF1α nuclear translocation. In conclusion, cP1P enhances the therapeutic potential of MSC through mTOR-dependent HIF1α translation and nuclear translocation.

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“…Moreover, it may be possible to control MSCs' fate in vitro and in vivo by regulating the ROS levels surrounding MSCs. Therefore, there is a great need to identify a promising strategy to prevent oxidative stress or pre‐invigoration of MSCs (C. Hu, Zhao, Peng, & Li, 2018). One of these strategies is the pretreatment of stem cells before their transplantation in damaged tissue and hypoxia condition.…”

Section: Discussionmentioning

confidence: 99%

Mitochondria‐targeted antioxidant mito‐TEMPO alleviate oxidative stress induced by antimycin A in human mesenchymal stem cells

Nouri

Gueguen

Saeedi

et al. 2020

Journal Cellular Physiology

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The cell therapy of damaged tissue, which is linked to hypoxia condition might fail, in large part due to the emergence of oxidative stress (OS) and/or mitochondrial dysfunctions. Thus, the invigoration of stem cells against oxidative stress could be a reliable strategy to improve the cell therapy outcome. Of various antioxidants, mito‐Tempo (mito‐T) is one of the potent antioxidants that could target and neutralize the mitochondrial oxidative stress. In this study, for the induction of hypoxia and oxidative stress in mitochondria of the mesenchymal stem cells (MSCs) isolated from human adipose tissue, antimycin A (AMA) was used and then several parameters were analyzed, including cell viability and cell cycle arrest of MSCs exposed to AMA, mito‐T, antioxidant potential, redox homeostasis, and signaling pathways in MSCs under oxidative stress. Based on our findings, the treated MSCs were found to impose a high resistance to the OS‐induced apoptosis, which correlated with the nuclear factor erythroid 2‐related factor 2 (Nrf2) pathway required to manage OS. Upon exposure of the MSCs to high oxidative stress conditions using AMA, the cells failed to scavenge. The use of mito‐T was found to alleviate the damage induced by oxidative stress through both direct functions of the free radical scavenging and the interplay in terms of cell signaling pathways including the upregulation of the Nrf2 pathway. These findings may pave the way in the stem cell therapy for the hypoxia‐mediated tissue damage.

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Regulation of the mitochondrial reactive oxygen species: Strategies to control mesenchymal stem cell fates ex vivo and in vivo

Cited by 54 publications

References 139 publications

Mitochondrial Dynamics: Fission and Fusion in Fate Determination of Mesenchymal Stem Cells

Mitochondrial Dynamics: Fission and Fusion in Fate Determination of Mesenchymal Stem Cells

O-cyclic phytosphingosine-1-phosphate stimulates HIF1α-dependent glycolytic reprogramming to enhance the therapeutic potential of mesenchymal stem cells

Mitochondria‐targeted antioxidant mito‐TEMPO alleviate oxidative stress induced by antimycin A in human mesenchymal stem cells

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