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Cells
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Mitochondrial Functions in Stem Cells
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Mitochondrial Functions in Stem Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Stem Cells".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 15916

Special Issue Editor

Dr. Alfonso Eirin

E-Mail Website
Guest Editor
Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA
Interests: renovascular disease; mitochondria; stem/progenitor cells; chronic kidney disease; obesity; hypertension; metabolic syndrome; extracellular vesicles

Special Issue Information

Dear Colleagues,

Regenerative cell-based therapies, such as infusion of stem cells or progenitor cells, have shown promising results in repairing damaged tissues in several organs. Mitochondria are intracellular organelles responsible for energy production that also regulate generation of reactive oxygen species, proliferation, apoptosis, and calcium homeostasis. Accumulating evidence suggests that mitochondria play critical roles in regulating multiple aspects of stem cell function, including their viability, plasticity, proliferative, and differential potential. However, the exact mechanisms by which these organelles modulate stem cell biology and function remain to be clarified. Understanding these mechanisms will aid the development of novel strategies to preserve mitochondrial structure and function and improve the efficacy and regenerative capacity of stem cells.

We invite investigators to contribute original research articles and review articles that help us to get more insight into the role of mitochondria in stem cell function and the development of strategies to preserve these organelles.

Potential topics include but are not limited to:

  • Experimental and clinical evidence of detrimental of mitochondrial structure, function, and viability in stem cells exposed to stress and noxious stimulus;
  • Influence of mitochondrial biogenesis, dynamics, and mitophagy on stem cell function;
  • Elucidating the role of mitochondrial oxidative stress in stem cell function;
  • Identifying markers of stem cell mitochondrial injury/dysfunction;
  • Recent advances in methods to assess stem cell mitochondrial function;
  • Novel therapeutic approaches to preserve stem cell mitochondrial structure and function;
  • Development of mitochondria-targeted therapies to preserve the regenerative potency of stem cells.

Dr. Alfonso Eirin
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Mitochondria
  • Stem Cells
  • Progenitor Cells
  • Cellular Energy
  • Oxidative Stress
  • Regenerative Medicine

Published Papers (4 papers)

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Research

Jump to: Review

16 pages, 3259 KiB  
Article
Renal Ischemia Induces Epigenetic Changes in Apoptotic, Proteolytic, and Mitochondrial Genes in Swine Scattered Tubular-like Cells
by Kamalnath S. Rajagopalan, Logan M. Glasstetter, Xiang-Yang Zhu, Roman Thaler, Hui Tang, Kyra L. Jordan, Ishran M. Saadiq, Sandra M. Herrmann, Alejandro R. Chade, Maria V. Irazabal, Lilach O. Lerman and Alfonso Eirin
Cells 2022, 11(11), 1803; https://doi.org/10.3390/cells11111803 - 31 May 2022
Cited by 6 | Viewed by 2115
Abstract
Background: Scattered tubular-like cells (STCs) are dedifferentiated renal tubular cells endowed with progenitor-like characteristics to repair injured parenchymal cells. STCs may be damaged and rendered ineffective by renal artery stenosis (RAS), but the underlying processes remain unclear. We hypothesized that RAS alters the [...] Read more.
Background: Scattered tubular-like cells (STCs) are dedifferentiated renal tubular cells endowed with progenitor-like characteristics to repair injured parenchymal cells. STCs may be damaged and rendered ineffective by renal artery stenosis (RAS), but the underlying processes remain unclear. We hypothesized that RAS alters the epigenetic landscape on DNA and the ensuing gene transcriptional profile of swine STCs. Methods: CD24+/CD133+ STCs were isolated from pig kidneys after 10 weeks of RAS or sham (n = 3 each) and their whole 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) profiles were examined by 5mC and 5hmC immunoprecipitation sequencing (MeDIP-/hMeDIP-seq, respectively). A subsequent integrated (MeDIP/hMeDIP-seq/mRNA-seq) analysis was performed by comparing all online available gene sets using Gene Set Enrichment Analysis. Apoptosis, proteolysis, and mitochondrial structure and function were subsequently evaluated in vitro. Results: Differential expression (DE) analysis revealed 239 genes with higher and 236 with lower 5mC levels and 275 genes with higher and 315 with lower 5hmC levels in RAS-STCs compared to Normal-STCs (fold change ≥1.4 or ≤0.7, p ≤ 0.05). Integrated MeDIP-/hMeDIP-seq/mRNA-seq analysis identified several overlapping (DE-5mC/mRNA and DE-5hmC/mRNA levels) genes primarily implicated in apoptosis, proteolysis, and mitochondrial functions. Furthermore, RAS-STCs exhibited decreased apoptosis, mitochondrial matrix density, and ATP production, and increased intracellular amino acid concentration and ubiquitin expression. Conclusions: Renal ischemia induces epigenetic changes in apoptosis-, proteolysis-, and mitochondria-related genes, which correlate with alterations in the transcriptomic profile and corresponding function of swine STCs. These observations may contribute to developing novel targeted interventions to preserve the reparative potency of STCs in renal disease. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Stem Cells)
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20 pages, 2588 KiB  
Article
The Mitochondrial Antioxidant Sirtuin3 Cooperates with Lipid Metabolism to Safeguard Neurogenesis in Aging and Depression
by Sónia Sá Santos, João B. Moreira, Márcia Costa, Rui S. Rodrigues, Ana M. Sebastião, Sara Xapelli and Susana Solá
Cells 2022, 11(1), 90; https://doi.org/10.3390/cells11010090 - 29 Dec 2021
Cited by 17 | Viewed by 3328
Abstract
Neural stem cells (NSCs), crucial for memory in the adult brain, are also pivotal to buffer depressive behavior. However, the mechanisms underlying the boost in NSC activity throughout life are still largely undiscovered. Here, we aimed to explore the role of deacetylase Sirtuin [...] Read more.
Neural stem cells (NSCs), crucial for memory in the adult brain, are also pivotal to buffer depressive behavior. However, the mechanisms underlying the boost in NSC activity throughout life are still largely undiscovered. Here, we aimed to explore the role of deacetylase Sirtuin 3 (SIRT3), a central player in mitochondrial metabolism and oxidative protection, in the fate of NSC under aging and depression-like contexts. We showed that chronic treatment with tert-butyl hydroperoxide induces NSC aging, markedly reducing SIRT3 protein. SIRT3 overexpression, in turn, restored mitochondrial oxidative stress and the differentiation potential of aged NSCs. Notably, SIRT3 was also shown to physically interact with the long chain acyl-CoA dehydrogenase (LCAD) in NSCs and to require its activation to prevent age-impaired neurogenesis. Finally, the SIRT3 regulatory network was investigated in vivo using the unpredictable chronic mild stress (uCMS) paradigm to mimic depressive-like behavior in mice. Interestingly, uCMS mice presented lower levels of neurogenesis and LCAD expression in the same neurogenic niches, being significantly rescued by physical exercise, a well-known upregulator of SIRT3 and lipid metabolism. Our results suggest that targeting NSC metabolism, namely through SIRT3, might be a suitable promising strategy to delay NSC aging and confer stress resilience. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Stem Cells)
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19 pages, 2213 KiB  
Article
Age-Related Changes in Bone-Marrow Mesenchymal Stem Cells
by Valentina A. Babenko, Denis N. Silachev, Tatyana I. Danilina, Kirill V. Goryunov, Irina B. Pevzner, Ljubava D. Zorova, Vasily A. Popkov, Valery P. Chernikov, Egor Y. Plotnikov, Gennady T. Sukhikh and Dmitry B. Zorov
Cells 2021, 10(6), 1273; https://doi.org/10.3390/cells10061273 - 21 May 2021
Cited by 18 | Viewed by 4438
Abstract
The use of stem cells is part of a strategy for the treatment of a large number of diseases. However, the source of the original stem cells for use is extremely important and determines their therapeutic potential. Mesenchymal stromal cells (MSC) have proven [...] Read more.
The use of stem cells is part of a strategy for the treatment of a large number of diseases. However, the source of the original stem cells for use is extremely important and determines their therapeutic potential. Mesenchymal stromal cells (MSC) have proven their therapeutic effectiveness when used in a number of pathological models. However, it remains an open question whether the chronological age of the donor organism affects the effectiveness of the use of MSC. The asymmetric division of stem cells, the result of which is some residential stem cells acquiring a non-senile phenotype, means that stem cells possess an intrinsic ability to preserve juvenile characteristics, implying an absence or at least remarkable retardation of senescence in stem cells. To test whether residential MSC senesce, we evaluated the physiological changes in the MSC from old rats, with a further comparison of the neuroprotective properties of MSC from young and old animals in a model of traumatic brain injury. We found that, while the effect of administration of MSC on lesion volume was minimal, functional recovery was remarkable, with the highest effect assigned to fetal cells; the lowest effect was recorded for cells isolated from adult rats and postnatal cells, having intermediate potency. MSC from the young rats were characterized by a faster growth than adult MSC, correlating with levels of proliferating cell nuclear antigen (PCNA). However, there were no differences in respiratory activity of MSC from young and old rats, but young cells showed much higher glucose utilization than old ones. Autophagy flux was almost the same in both types of cells, but there were remarkable ultrastructural differences in old and young cells. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Stem Cells)
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Review

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22 pages, 864 KiB  
Review
Mitochondrial Phenotypes in Parkinson’s Diseases—A Focus on Human iPSC-Derived Dopaminergic Neurons
by Leonie M. Heger, Rachel M. Wise, J. Tabitha Hees, Angelika B. Harbauer and Lena F. Burbulla
Cells 2021, 10(12), 3436; https://doi.org/10.3390/cells10123436 - 07 Dec 2021
Cited by 6 | Viewed by 5140
Abstract
Established disease models have helped unravel the mechanistic underpinnings of pathological phenotypes in Parkinson’s disease (PD), the second most common neurodegenerative disorder. However, these discoveries have been limited to relatively simple cellular systems and animal models, which typically manifest with incomplete or imperfect [...] Read more.
Established disease models have helped unravel the mechanistic underpinnings of pathological phenotypes in Parkinson’s disease (PD), the second most common neurodegenerative disorder. However, these discoveries have been limited to relatively simple cellular systems and animal models, which typically manifest with incomplete or imperfect recapitulation of disease phenotypes. The advent of induced pluripotent stem cells (iPSCs) has provided a powerful scientific tool for investigating the underlying molecular mechanisms of both familial and sporadic PD within disease-relevant cell types and patient-specific genetic backgrounds. Overwhelming evidence supports mitochondrial dysfunction as a central feature in PD pathophysiology, and iPSC-based neuronal models have expanded our understanding of mitochondrial dynamics in the development and progression of this devastating disorder. The present review provides a comprehensive assessment of mitochondrial phenotypes reported in iPSC-derived neurons generated from PD patients’ somatic cells, with an emphasis on the role of mitochondrial respiration, morphology, and trafficking, as well as mitophagy and calcium handling in health and disease. Furthermore, we summarize the distinguishing characteristics of vulnerable midbrain dopaminergic neurons in PD and report the unique advantages and challenges of iPSC disease modeling at present, and for future mechanistic and therapeutic applications. Full article
(This article belongs to the Special Issue Mitochondrial Functions in Stem Cells)
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