ROS and Oxidative Stress in Stem Cells Cieślar-Pobuda ... · This is an open access article...

ROS and Oxidative Stress in Stem Cells

Cieślar-Pobuda, Artur; Yue, Jianbo; Lee, Hsin-Chen; Skonieczna, Magdalena; Wei, Yau-Huei

Published in:Oxidative Medicine and Cellular Longevity

Published: 06/09/2017

Document Version:Final Published version, also known as Publisher’s PDF, Publisher’s Final version or Version of Record

License:CC BY

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Published version (DOI):10.1155/2017/5047168

Publication details:Cieślar-Pobuda, A., Yue, J., Lee, H-C., Skonieczna, M., & Wei, Y-H. (2017). ROS and Oxidative Stress in StemCells. Oxidative Medicine and Cellular Longevity, 2017, [5047168]. https://doi.org/10.1155/2017/5047168

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https://doi.org/10.1155/2017/5047168

EditorialROS and Oxidative Stress in Stem Cells

Artur Cieślar-Pobuda,1 Jianbo Yue,2 Hsin-Chen Lee,3 Magdalena Skonieczna,4 andYau-Huei Wei3,5

1Stem Cell Group, Nordic EMBL Partnership, Centre for Molecular Medicine Norway (NCMM), University of Oslo, Oslo, Norway2City University of Hong Kong, Kowloon, Hong Kong3Center for Mitochondrial Medicine and Free Radical Research, Changhua Christian Hospital, Changhua City, Taiwan4Biotechnology Centre, Silesian University of Technology, Gliwice, Poland5Mackay Medical College, New Taipei City, Taiwan

Correspondence should be addressed to Artur Cieślar-Pobuda; [email protected]

Received 19 June 2017; Accepted 20 June 2017; Published 6 September 2017

Copyright © 2017 Artur Cieślar-Pobuda et al. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the originalwork is properly cited.

Reactive oxygen species (ROS) are well known to be impli-cated in various important cellular processes including sig-naling, regulation of homeostasis, or induction of death.Oxidative stress resulting from increased ROS productionand impaired free radical scavenging systems can causesevere damage to biological macromolecules, affecting cellproliferation and causing genomic instability and cellularsenescence. Although ROS are involved in a wide range ofcellular processes, a limited number of studies have exam-ined the generation and function of ROS in stem cells. Itis known that ROS may enhance differentiation of stemcells and facilitate reprogramming into induced pluripotentstem cells (iPSCs), but on the other hand, they are alsoassociated with malignant transformation or prematureaging. Stem cells have also been shown to possess defectiveDNA repair machinery, which may have serious conse-quences for cells exposed to extensive oxidative stress. Sincestem cells are considered as a promising tool in regenera-tive medicine, it is crucial to know and better understandall the processes related to ROS to prevent potential gener-ation of mutations causing genomic instability and to avoidunwanted ROS-driven differentiation. Thus, the mecha-nisms by which genomic integrity of stem cells is main-tained under oxidative stress and the role of ROS should

be elucidated before stem cells finally find their place inclinical applications.

The paper by C.-J. Li et al. demonstrates that treatmentwith antioxidants not only increases proliferation andmitochondrial integrity of human mesenchymal stem cells(hMSCs) but also enhances the therapeutic potential ofhMSCs by promoting the formation of tunneling nanotubes(TNTs) between hMSCs and oxidatively injured cells in acoculture system. The authors demonstrate that TNTs enablehMSCs to “export” their healthy mitochondria to the injuredcells and hence decrease their oxidative stress and stabilizethe mitochondrial membrane potential of the injured cells.Concurrently, the rescued cells also show enhanced mito-phagy, implicating that their damaged mitochondria areeliminated in order to maintain normal cell physiology. Thefindings highlight that antioxidants enhance mitochondrialtransfer from hMSCs to the injured cells and provide themwith a repair mechanism.

A similar topic is presented by Y.-C. Chuang et al.who show that Wharton’s jelly mesenchymal stem cells(WJMSCs) are able to transfer healthy mitochondria tocybrid cells from a patient with myoclonus epilepsy associ-ated with ragged-red fibers (MERRF) through intercellularconnections. This mitochondrial transfer is found to be

HindawiOxidative Medicine and Cellular LongevityVolume 2017, Article ID 5047168, 2 pageshttps://doi.org/10.1155/2017/5047168

https://doi.org/10.1155/2017/5047168

associated with reduction of oxidative stress and improve-ment of mitochondrial bioenergetics in MERRF cybrid cells.The ability of WJMSCs to “help” cells with defective mito-chondrial function (e.g., MERRF cells) through donatinghealthy mitochondria is an intriguing phenomenon thatmay provide new cues for the development of more effec-tive treatment of diseases caused by or associated withmitochondrial dysfunction.

V. A. Sergeeva et al. contributed an interesting study, inwhich the adaptive response of MSCs to low doses of ionizingradiation (IR) is described. The authors show that such aresponse may be mediated by oxidized cell-free DNA(cfDNA) fragments. It is demonstrated that treatment ofMSCs with low doses of IR leads to cell death of part ofthe cell population and release of oxidized cfDNA, whichhas the ability to penetrate into the cytoplasm of othercells. Oxidized cfDNA, like low doses of IR, induces ROSproduction, ROS-induced oxidative DNA damage, cellcycle arrest, activation of DNA repair mechanisms, andinhibition of apoptosis. The MSCs pretreated with a lowdose of irradiation or oxidized cfDNA are equally effectivein induction of an adaptive response to the challenge offurther doses of radiation. This study suggests that oxidizedcfDNA is a stress-triggered signaling molecule that mediatesradiation-induced bystander effects and that it is an impor-tant component of radioadaptive responses of cells to lowdoses of IR.

D. Sainz de la Maza et al. explore the role of ROS andautophagy on reprogramming of primordial germ cells(PGCs) into pluripotent cells. The authors demonstrate thata metabolic shift from oxidative phosphorylation toward gly-colysis, autophagy, and mitochondrial inactivation and anearly rise in ROS levels are necessary for PGC reprogram-ming. It is shown that all these processes are regulated by acorrect (right) HIF1/HIF2 balance and Oct4. The cellsobtained are unable to self-renew, and it is postulated thatBlimp1 may be responsible for this.

J. Kučera et al. focus in their work on the effect ofhypoxia on intracellular signaling pathways responsiblefor mouse embryonic stem (ES) cell maintenance. Byemploying wild-type and hypoxia inducible factor 1-(HIF-1-) deficient ES cells and measuring phosphorylationof proteins of the ERK, Akt, and STAT3 pathways, theauthors investigate the response of ES cells to hypoxia.The study shows that ERK signaling is downregulated inhypoxia in a ROS-dependent manner, but without theinvolvement of hypoxia-inducible factor HIF-1. Theauthors also observe a decreased ROS level in hypoxiaand a similar phosphorylation pattern for ERK when thecells are supplemented with glutathione.

Finally, the review article by M. Skonieczna et al. givesan extensive overview about NADPH oxidases (NOX) andtheir role in various cellular systems. The article describesthe functions and mechanisms of action of NOX andNOX-derived ROS in stem cells, cancer cells, and cancerstem cells. It also points out the importance of understandingNOX-dependent cellular processes, as a future perspectivefor regenerative medicine and development of new therapiestoward cancers.

In conclusion, the aim of this special issue is to provideupdated information for readers to better understand therole of oxidative stress and ROS in stem cell physiology.All the articles selected for this special issue presentimportant findings that will undoubtedly provide usefulcues for future research.

Artur Cieślar-PobudaJianbo Yue

Hsin-Chen LeeMagdalena Skonieczna

Yau-Huei Wei

2 Oxidative Medicine and Cellular Longevity

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