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Article

MIT-001 Restores Human Placenta-Derived Mesenchymal Stem Cells by Enhancing Mitochondrial Quiescence and Cytoskeletal Organization

1
Department of Biomedical Science, College of Life Science, CHA University, Pocheon 11160, Korea
2
CHA Fertility Center, Seoul Station, Hangang-daero, Jung-gu, Seoul 04637, Korea
3
Mitoimmune Therapeutics Inc., Gangnam-gu, Seoul 06253, Korea
*
Authors to whom correspondence should be addressed.
Academic Editor: Monia Orciani
Int. J. Mol. Sci. 2021, 22(10), 5062; https://doi.org/10.3390/ijms22105062
Received: 19 April 2021 / Revised: 4 May 2021 / Accepted: 6 May 2021 / Published: 11 May 2021
Inflammation is a major cause of several chronic diseases and is reported to be recovered by the immuno-modulation of mesenchymal stem cells (MSCs). While most studies have focussed on the anti-inflammatory roles of MSCs in stem cell therapy, the impaired features of MSCs, such as the loss of homeostasis by systemic aging or pathologic conditions, remain incompletely understood. In this study, we investigated whether the altered phenotypes of human placenta-derived MSCs (hPD-MSCs) exposed to inflammatory cytokines, including TNF-α and IFN-γ, could be protected by MIT-001, a small anti-inflammatory and anti-necrotic molecule. MIT-001 promoted the spindle-like shape and cytoskeletal organization extending across the long cell axis, whereas hPD-MSCs exposed to TNF-α/IFN-γ exhibited increased morphological heterogeneity with an abnormal cell shape and cytoskeletal disorganization. Importantly, MIT-001 improved mitochondrial distribution across the cytoplasm. MIT-001 significantly reduced basal respiration, ATP production, and cellular ROS levels and augmented the spare respiratory capacity compared to TNF-α/IFN-γ-exposed hPD-MSCs, indicating enhanced mitochondrial quiescence and homeostasis. In conclusion, while TNF-α/IFN-γ-exposed MSCs lost homeostasis and mitochondrial quiescence by becoming over-activated in response to inflammatory cytokines, MIT-001 was able to rescue mitochondrial features and cellular phenotypes. Therefore, MIT-001 has therapeutic potential for clinical applications to treat mitochondrion-related inflammatory diseases. View Full-Text
Keywords: mesenchymal stem cells; inflammation; homeostasis; mitochondria; cytoskeleton; MIT-001 mesenchymal stem cells; inflammation; homeostasis; mitochondria; cytoskeleton; MIT-001
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MDPI and ACS Style

Yu, W.D.; Kim, Y.J.; Cho, M.J.; Kim, G.J.; Kim, S.H.; Kim, M.J.; Ko, J.J.; Lee, J.H. MIT-001 Restores Human Placenta-Derived Mesenchymal Stem Cells by Enhancing Mitochondrial Quiescence and Cytoskeletal Organization. Int. J. Mol. Sci. 2021, 22, 5062. https://doi.org/10.3390/ijms22105062

AMA Style

Yu WD, Kim YJ, Cho MJ, Kim GJ, Kim SH, Kim MJ, Ko JJ, Lee JH. MIT-001 Restores Human Placenta-Derived Mesenchymal Stem Cells by Enhancing Mitochondrial Quiescence and Cytoskeletal Organization. International Journal of Molecular Sciences. 2021; 22(10):5062. https://doi.org/10.3390/ijms22105062

Chicago/Turabian Style

Yu, Won D., Yu J. Kim, Min J. Cho, Gi J. Kim, Soon H. Kim, Myung J. Kim, Jung J. Ko, and Jae H. Lee. 2021. "MIT-001 Restores Human Placenta-Derived Mesenchymal Stem Cells by Enhancing Mitochondrial Quiescence and Cytoskeletal Organization" International Journal of Molecular Sciences 22, no. 10: 5062. https://doi.org/10.3390/ijms22105062

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