Cited by 242Mitochondrial Function and PathologyMesenchymal stem cell researchAutophagy in Disease and Therapy

Miro1 Enhances Mitochondria Transfer from Multipotent Mesenchymal Stem Cells (MMSC) to Neural Cells and Improves the Efficacy of Cell Recovery

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Babenko, Valentina, Silachev, Denis, Popkov, Vasily, Zorova, Ljubava, Pevzner, Irina, Plotnikov, Egor, Sukhikh, Gennady, Zorov, Dmitry·2018·Molecules

Abstract

A recently discovered key role of reactive oxygen species (ROS) in mitochondrial traffic has opened a wide alley for studying the interactions between cells, including stem cells. Since its discovery in 2006, intercellular mitochondria transport has been intensively studied in different cellular models as a basis for cell therapy, since the potential of replacing malfunctioning organelles appears to be very promising. In this study, we explored the transfer of mitochondria from multipotent mesenchymal stem cells (MMSC) to neural cells and analyzed its efficacy under normal conditions and upon induction of mitochondrial damage. We found that mitochondria were transferred from the MMSC to astrocytes in a more efficient manner when the astrocytes were exposed to ischemic damage associated with elevated ROS levels. Such transport of mitochondria restored the bioenergetics of the recipient cells and stimulated their proliferation. The introduction of MMSC with overexpressed Miro1 in animals that had undergone an experimental stroke led to significantly improved recovery of neurological functions. Our data suggest that mitochondrial impairment in differentiated cells can be compensated by receiving healthy mitochondria from MMSC. We demonstrate a key role of Miro1, which promotes the mitochondrial transfer from MMSC and suggest that the genetic modification of stem cells can improve the therapies for the injured brain.

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  • Genetic modification of key molecular mediators such as Miro1 and CX43 represents a direct and well-supported strategy to optimize the mitochondrial transfer efficiency of MSCs.

    “Genetic modification of key molecular mediators responsible for triggering and regulating MT, such as mitochondrial Rho-GTPase 1 (Miro1) and connexin 43 (CX43), represents a direct and well-supported strategy to optimize the MT efficiency of MSCs [392–394].”

    From Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells (2025) · cites this paper as [392]

    The Results (§2.4; page not provided) report that Miro1-overexpressing MMSCs transferred more mitochondria to astrocytes, supporting genetic modification of Miro1 as a way to improve transfer efficiency. The cited paper does not establish the corresponding claim for CX43, which is also included in the sentence attributed to the citation group. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Miro1 is a calcium-sensitive adaptor protein that attaches mitochondria to the KIF5 motor protein and other accessory proteins like Miro2, TRAK1, TRAK2, and Myo19, thus aiding mitochondrial movement along microtubules.

    “Miro1 is a calcium-sensitive adaptor protein that attaches the Mt to the KIF5 motor protein and other accessory proteins like Miro2, TRAK1, TRAK2, and Myo19, thus aiding Mt movement along microtubules [392, 393].”

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Cited by

Sorted by citations

Authors
Babenko, V., Silachev, D., Popkov, V., Zorova, L., Pevzner, I., Plotnikov, E., Sukhikh, G., & Zorov, D.
Affiliations
  • Lomonosov Moscow State University (RU)
  • Sechenov University (RU)
Corresponding author
  • Plotnikov, Egor
  • Zorov, Dmitry
Venue
Molecules
Publisher
MDPI AG
Published
2018-03-19
Volume
23
Issue
3
Pages
687
ISSN
1420-3049 (ISSN-L)
OpenAlex
W2791535752
Cited by
242
References
5
Citations by year
2026: 32 · 2025: 31 · 2024: 40 · 2023: 37 · 2022: 29 · 2021: 25 · 2020: 28 · 2019: 12 · 2018: 8
FWCI
6.49
Type
journal article
Language
en
Open access
Locations
  • Molecules (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Grant of the President (MD-2065.2018.4)
  • Russian Science Foundation (14-15-00147)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
Miro1, mitochondrial transfer, astrocytes, reactive oxygen species, ischemic brain injury, stroke recovery, mitochondrial damage, cell therapy, bioenergetics, cell proliferation
MeSH terms
Animals, Astrocytes, Humans, Mitochondria, Neurons, PC12 Cells, Cell Respiration, rho GTP-Binding Proteins, Mitochondrial Proteins, Multipotent Stem Cells, Nanotubes, Cell Proliferation, Rats, Mesenchymal Stem Cells

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