Intercellular transfer of mitochondria

Plotnikov, Egor Y.; Babenko, Valentina A.; Silachev, D. N.; Zorova, Ljubava D.; Khryapenkova, T. G.; Savchenko, E. S.; Pevzner, Irina B.; Zorov, Dmitry B.

doi:10.1134/s0006297915050041

Cited by 26 publications

(25 citation statements)

References 50 publications

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“…Organelle movement between mammalian cells in culture via tunneling membrane nanotubes was first demonstrated by Gerdes' group and intercellular mitochondrial transfer was shown soon after . During the following decade, mitochondrial transfer between cells has been confirmed in many human and rodent cell culture systems in vitro …”

Section: Mitochondrial Trafficking Between Cells In Culturementioning

confidence: 95%

The mobility of mitochondria: Intercellular trafficking in health and disease

Berridge

Neužil

2017

Clin Exp Pharma Physio

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SummaryThe view that genes are constrained within somatic cells is challenged by in vitro evidence, and more recently by in vivo studies which demonstrate that mitochondria with their mitochondrial DNA (mtDNA) payload not only can, but do move between cells in tumour models and in mouse models of tissue damage. Using mouse tumour cell models without mtDNA to reflect mtDNA damage, we have shown that these cells | THE ORIGIN OF MITOCHONDRIARemarkable progress has been made over the last few years in firmly establishing the cellular origins of mitochondria present in almost all complex organisms. Although there is general consensus that the bacterium giving rise to mitochondria was an α-proteobacterium capable of using low levels oxygen present in the Proterozoic environment to generate chemical energy in the form of ATP, the nature of the engulfing organism has been more controversial. The discovery of Lokiarchaeota in deep sea sediments off the Icelandic coast 1 and subsequent elaboration of Asgard archaea 2 support the view that a highly evolved archaeal cell with many primitive eukaryotic features was the symbiont that hosted the mitochondrial precursor cell, and this appears to have been a singular event. It is noteworthy that both α-proteobacteria and archaea are capable forming pilli-like structures that transmit genetic material between cells, and that these properties

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Section: Mitochondrial Trafficking Between Cells In Culturementioning

confidence: 95%

The mobility of mitochondria: Intercellular trafficking in health and disease

Berridge

Neužil

2017

Clin Exp Pharma Physio

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“…Different techniques emerged to mimic the natural transfer or mitochondria on its in vivo and in vitro applications. The coincubation technique was the first proposed in which the antibiotic resistance carried in the mitochondrial DNA was passed to sensitive cells [9], later after the technique was used to rescue respiratory deficient cells among other damaged cells [10, 11, 14, 63]. Microinjection of exogenous mitochondria was applied in assays to eliminate the endogenous copies of oocytes carrying mitochondrial diseases [90, 93].…”

Section: Figurementioning

confidence: 99%

Artificial Mitochondria Transfer: Current Challenges, Advances, and Future Applications

Caicedo

Aponte

Cabrera

et al. 2017

Stem Cells International

112

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The objective of this review is to outline existing artificial mitochondria transfer techniques and to describe the future steps necessary to develop new therapeutic applications in medicine. Inspired by the symbiotic origin of mitochondria and by the cell's capacity to transfer these organelles to damaged neighbors, many researchers have developed procedures to artificially transfer mitochondria from one cell to another. The techniques currently in use today range from simple coincubations of isolated mitochondria and recipient cells to the use of physical approaches to induce integration. These methods mimic natural mitochondria transfer. In order to use mitochondrial transfer in medicine, we must answer key questions about how to replicate aspects of natural transport processes to improve current artificial transfer methods. Another priority is to determine the optimum quantity and cell/tissue source of the mitochondria in order to induce cell reprogramming or tissue repair, in both in vitro and in vivo applications. Additionally, it is important that the field explores how artificial mitochondria transfer techniques can be used to treat different diseases and how to navigate the ethical issues in such procedures. Without a doubt, mitochondria are more than mere cell power plants, as we continue to discover their potential to be used in medicine.

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“…[7][8][9] Complementation thereby is not restricted to one cell but can occur across different cells via tunneling nanotubes and extracellular vesicles. [10][11][12] Further, fission and selective fusion can sort out nonfunctional mitochondria which are tagged by PINK1/parkin for lysosomal degradation (i.e., mitophagy). [13][14][15][16][17] Mitophagy is a way to recycle damaged or superfluous mitochondria, for example during erythrocyte maturation, mediated by several different receptors, such as BNIP3, BNIP3L, FUNDC1, and MCL1.…”

Section: Mitochondriamentioning

confidence: 99%

“…For example, fusion with wild‐type mitochondria can attenuate mtDNA mutations through cross‐complementation between organelles . Complementation thereby is not restricted to one cell but can occur across different cells via tunneling nanotubes and extracellular vesicles . Further, fission and selective fusion can sort out nonfunctional mitochondria which are tagged by PINK1/parkin for lysosomal degradation (i.e., mitophagy) .…”

Section: Introductionmentioning

confidence: 99%

Targeted OMA1 therapies for cancer

Alavi¹

2019

Intl Journal of Cancer

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The mitochondrial inner membrane proteins OMA1 and OPA1 belong to the BAX/BAK1‐dependent apoptotic signaling pathway, which can be regulated by tumor protein p53 and the prohibitins PHB and PHB2 in the context of neoplastic disease. For the most part these proteins have been studied separate from each other. Here, I argue that the OMA1 mechanism of action represents the missing link between p53 and cytochrome c release. The mitochondrial fusion protein OPA1 is cleaved by OMA1 in a stress‐dependent manner generating S‐OPA1. Excessive S‐OPA1 can facilitate outer membrane permeabilization upon BAX/BAK1 activation through its membrane shaping properties. p53 helps outer membrane permeabilization in a 2‐step process. First, cytosolic p53 activates BAX/BAK1 at the mitochondrial surface. Then, in a second step, p53 binds to prohibitin thereby releasing the restraint on OMA1. This activates OMA1, which cleaves OPA1 and promotes cytochrome c release. Clearly, OMA1 and OPA1 are not root causes for cancer. Yet many cancer cells rely on this pathway for survival, which can explain why loss of p53 function promotes tumor growth and confers resistance to chemotherapies.

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Intercellular transfer of mitochondria

Cited by 26 publications

References 50 publications

The mobility of mitochondria: Intercellular trafficking in health and disease

The mobility of mitochondria: Intercellular trafficking in health and disease

Artificial Mitochondria Transfer: Current Challenges, Advances, and Future Applications

Targeted OMA1 therapies for cancer

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