Correction: Corrigendum: Transfer of mitochondria from astrocytes to neurons after stroke

Hayakawa, Kazuhide; Esposito, Elga; Wang, Xiaohua; Terasaki, Yasukazu; Liu, Yi; Xing, Chao; Ji, Xunming; Lo, Eng H.

doi:10.1038/nature19805

Cited by 20 publications

(16 citation statements)

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“…Importantly, stem cells are recognized as unexceptionable donor cells for mitochondrial transfer and numerous studies have substantiated the significance of mitochondrial transfer in stem cell therapy, especially mesenchymal stem cells 23. Mitochondria could be transferred from mesenchymal stem cells to nearby injured cells to improve cell viability 24, 25.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

et al. 2019

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Recent studies have demonstrated that bone marrow mesenchymal stem cells (BMSCs) protect the injured neurons of spinal cord injury (SCI) from apoptosis while the underlying mechanism of the protective effect of BMSCs remains unclear. In this study, we found the transfer of mitochondria from BMSCs to injured motor neurons and detected the functional improvement after transplanting. Methods: Primary rat BMSCs were co-cultured with oxygen-glucose deprivation (OGD) injured VSC4.1 motor neurons or primary cortical neurons. FACS analysis was used to detect the transfer of mitochondria from BMSCs to neurons. The bioenergetics profiling of neurons was detected by Extracellular Flux Analysis. Cell viability and apoptosis were also measured. BMSCs and isolated mitochondria were transplanted into SCI rats. TdT-mediated dUTP nick end labelling staining was used to detect apoptotic neurons in the ventral horn. Immunohistochemistry and Western blotting were used to measure protein expression. Re-myelination was examined by transmission electron microscope. BBB scores were used to assess locomotor function. Results: MitoTracker-Red labelled mitochondria of BMSCs could be transferred to the OGD injured neurons. The gap junction intercellular communication (GJIC) potentiator retinoid acid increased the quantity of mitochondria transfer from BMSCs to neurons, while GJIC inhibitor 18β glycyrrhetinic acid decreased mitochondria transfer. Internalization of mitochondria improved the bioenergetics profile, decreased apoptosis and promoted cell survival in post-OGD motor neurons. Furthermore, both transplantation of mitochondria and BMSCs to the injured spinal cord improved locomotor functional recovery in SCI rats. Conclusions: To our knowledge, this is the first evidence that BMSCs protect against SCI through GJIC to transfer mitochondrial to the injured neurons. Our findings suggested a new therapy strategy of mitochondria transfer for the patients with SCI.

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Section: Introductionmentioning

confidence: 99%

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

et al. 2019

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“…One unexpected finding that provides a new perspective on mitochondrial biology is based on the observation that these interesting organelles can be secreted from the cell and can be transferred to neighboring cells [98][99][100] . As we explained in the beginning of this review, mitochondria originated evolutionarily from independently living bacteria.…”

Section: Perspective and Conclusionmentioning

confidence: 99%

Molecular cross talk among the components of the regulatory machinery of mitochondrial structure and quality control

Cho

Sun

2020

Exp Mol Med

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Mitochondrial dysfunction critically impairs cellular health and often causes or affects the progression of several diseases, including neurodegenerative diseases and cancer. Thus, cells must have several ways to monitor the condition of mitochondrial quality and maintain mitochondrial health. Accumulating evidence suggests that the molecular machinery responding to spontaneous changes in mitochondrial morphology is associated with the routine mitochondrial quality control system. In this short review, we discuss recent progress made in linking mitochondrial structural dynamics and the quality control system.

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“…In addition to transcellular mitophagy, the observation of glial cells transferring mitochondria to neurons has been documented. In stroke models, glial cells transfer mitochondria to neurons as a likely means to protect neurons from energy stress and hypoxia [85,86]. The specific pathways which facilitate mitochondrial transfer between cells are unknown.…”

Section: Transcellular Mitophagymentioning

confidence: 99%

Mitophagy and the Brain

Swerdlow

Wilkins

2020

Preprint

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Stress mechanisms have long been associated with neuronal loss and neurodegenerative diseases. The origin of cell stress and neuronal loss likely stems from multiple pathways. These include (but are not limited to) bioenergetic failure, neuroinflammation, and loss of proteostasis. Cells have adapted compensatory mechanisms to overcome stress and circumvent death. One mechanism is mitophagy. Recent studies have implicated mitophagy in several neurodegenerative diseases and clinical trials are underway which target mitophagy pathways. Here, we review mitophagy pathways, the role of mitophagy in neurodegeneration, potential therapeutics, and the need for further study.

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Correction: Corrigendum: Transfer of mitochondria from astrocytes to neurons after stroke

Abstract: In this Letter, in Fig. 1d and 1m, the y axis label should have read 'JC1 (red/green)' instead of 'JC1 (green/red)'; this has been corrected online.

Cited by 20 publications

References 1 publication

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

Mitochondrial Transfer from Bone Marrow Mesenchymal Stem Cells to Motor Neurons in Spinal Cord Injury Rats via Gap Junction

Molecular cross talk among the components of the regulatory machinery of mitochondrial structure and quality control

Mitophagy and the Brain

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