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Mitochondrial transfer from mesenchymal stem cells to neural stem cells protects against the neurotoxic effects of cisplatin. | LitMetric

Mitochondrial transfer from mesenchymal stem cells to neural stem cells protects against the neurotoxic effects of cisplatin.

Acta Neuropathol Commun

Laboratory of Neuroimmunology, Department of Symptom Research, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 384, Houston, TX, 77030, USA.

Published: December 2018

AI Article Synopsis

  • Mesenchymal stem cells (MSCs) can transfer healthy mitochondria to damaged neural stem cells (NSCs) using actin-based structures, providing protection against cell damage from cisplatin. !* -
  • The study found that when MSCs donated mitochondria to NSCs exposed to cisplatin, it reduced NSC death and improved mitochondrial function. !* -
  • In animal models, MSC treatment helped prevent the loss of neural progenitor cells caused by cisplatin, suggesting that mitochondrial transfer is a key mechanism behind the MSCs' protective effects. !*

Article Abstract

Mesenchymal stem cells (MSCs) transfer healthy mitochondria to damaged acceptor cells via actin-based intercellular structures. In this study, we tested the hypothesis that MSCs transfer mitochondria to neural stem cells (NSCs) to protect NSCs against the neurotoxic effects of cisplatin treatment. Our results show that MSCs donate mitochondria to NSCs damaged in vitro by cisplatin. Transfer of healthy MSC-derived mitochondria decreases cisplatin-induced NSC death. Moreover, mitochondrial transfer from MSCs to NSCs reverses the cisplatin-induced decrease in mitochondrial membrane potential. Blocking the formation of actin-based intercellular structures inhibited the transfer of mitochondria to NSCs and abrogated the positive effects of MSCs on NSC survival. Conversely, overexpression of the mitochondrial motor protein Rho-GTPase 1 (Miro1) in MSCs increased mitochondrial transfer and further improved survival of cisplatin-treated NSCs.In vivo, MSC administration prevented the loss of DCX+ neural progenitor cells in the subventricular zone and hippocampal dentate gyrus which occurs as a result of cisplatin treatment. We propose mitochondrial transfer as one of the mechanisms via which MSCs exert their therapeutic regenerative effects after cisplatin treatment.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292021PMC
http://dx.doi.org/10.1186/s40478-018-0644-8DOI Listing

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