Long range physical cell-to-cell signalling via mitochondria inside membrane nanotubes: a hypothesis

Scholkmann, Felix

doi:10.1186/s12976-016-0042-5

Cited by 38 publications

(26 citation statements)

References 192 publications

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“…Furthermore, as increased generation of ROS is a hallmark of many diseases as diverse as neurodegeneration, diabetes, and cancer, UPE stimulation of excitonic transport in microtubules may represent a coherent signaling mechanism at the root of multiple aging processes. Supporting this line of thought, recent evidence [58] confirms the existence of "membrane nanotubes" containing Factin and microtubules, which may serve as a means of long-range cell-to-cell signaling-a kind of intercellular highway. These nanotubes facilitate cell-to-cell communication through a diverse array of methods, ranging from the exchange of a variety of signaling carriers, organelles, and even unicellular organisms, to the enabling of long-distance electrical coupling between cells.…”

Section: Discussionmentioning

confidence: 80%

Oxidative species-induced excitonic transport in tubulin aromatic networks: Potential implications for neurodegenerative disease

Kurian

Obisesan

Craddock

2017

Journal of Photochemistry and Photobiology B: Biology

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Oxidative stress is a pathological hallmark of neurodegenerative tauopathic disorders such as Alzheimer’s disease and Parkinson’s disease-related dementia, which are characterized by altered forms of the microtubule-associated protein (MAP) tau. MAP tau is a key protein in stabilizing the microtubule architecture that regulates neuron morphology and synaptic strength. When MAP tau is degraded in tauopathic disorders, neuron dysfunction results. The precise role of reactive oxygen species (ROS) in the tauopathic disease process, however, is poorly understood. Classically, mitochondrial dysfunction has been viewed as the major source of oxidative stress and has been shown to precede tau and amyloid pathology in various dementias, but the exact mechanisms are not clear. It is known that the production of ROS by mitochondria can result in ultraweak photon emission (UPE) within cells. While of low intensity, surrounding proteins within the cytosol can still absorb these energetic photons via aromatic amino acids (e.g., tryptophan and tyrosine). One likely absorber of these photons is the microtubule cytoskeleton, as it forms a vast network spanning neurons, is highly colocalized with mitochondria, and shows a high density of aromatic amino acids. Functional microtubule networks may traffic this ROS-generated endogenous photon energy for cellular signaling, or they may serve as dissipaters/conduits of such energy to protect the cell from potentially harmful effects. Experimentally, after in vitro exposure to exogenous photons, microtubules have been shown to reorient and reorganize in a dose-dependent manner with the greatest effect being observed around 280 nm, in the tryptophan and tyrosine absorption range. In this paper, recent modeling efforts based on ambient temperature experiment are presented, showing that tubulin polymers can feasibly absorb and channel these photoexcitations via resonance energy transfer, on the order of dendritic length scales and neuronal fine structure. Since microtubule networks are compromised in tauopathic diseases such as Alzheimer’s and Parkinson’s dementias, patients with these illnesses would be unable to support effective channeling of these photons for signaling or dissipation. Consequent emission surplus due to increased UPE production or decreased ability to absorb and transfer may lead to increased cellular oxidative damage, thus hastening the neurodegenerative process.

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Section: Discussionmentioning

confidence: 80%

Oxidative species-induced excitonic transport in tubulin aromatic networks: Potential implications for neurodegenerative disease

Kurian

Obisesan

Craddock

2017

Journal of Photochemistry and Photobiology B: Biology

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“…Another possibility is that fusion could confer robustness to the mitochondrial pool by dampening biochemical fluctuations (Mai et al, 2010) and by allowing functional complementation through the exchange of mitochondrial contents (Nakada et al, 2001; Ono et al, 2001). Fusion may also protect healthy mitochondria from being targeted for degradation (Twig et al, 2008) or enable efficient energy transmission along intracellular power cables constituted by filamentous mitochondria (Amchenkova et al, 1988; Glancy et al, 2015; Scholkmann, 2016; Skulachev, 2001) (see section 5 ).…”

Section: Nanotubulation-reticulationmentioning

confidence: 99%

“…Motile mitochondria are present not only within cells but may also be present between cells. Recent studies have observed mitochondria inside microtubule-containing ‘membrane nanotubes’ connecting neighboring cells (Antanaviciute et al, 2014; Liu and Hajnoczky, 2011; Lu et al, 2017; Scholkmann, 2016). Endogenous and expressed Bcl-xL in neurons increases the number of synapses that contain a mitochondrion immediately adjacent to the synaptic density (Li et al, 2013; Li et al, 2008).…”

Section: Descriptions Of Mitochondrial Morphologymentioning

confidence: 99%

Connecting mitochondrial dynamics and life-or-death events via Bcl-2 family proteins

Aouacheria

Baghdiguian

Lamb

et al. 2017

Neurochemistry International

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The morphology of a population of mitochondria is the result of several interacting dynamical phenomena, including fission, fusion, movement, elimination and biogenesis. Each of these phenomena is controlled by underlying molecular machinery, and when defective can cause disease. New understanding of the relationships between form and function of mitochondria in health and disease is beginning to be unraveled on several fronts. Studies in mammals and model organisms have revealed that mitochondrial morphology, dynamics and function appear to be subject to regulation by the same proteins that regulate apoptotic cell death. One protein family that influences mitochondrial dynamics in both healthy and dying cells is the Bcl-2 protein family. Connecting mitochondrial dynamics with life-death pathway forks may arise from the intersection of Bcl-2 family proteins with the proteins and lipids that determine mitochondrial shape and function. Bcl-2 family proteins also have multifaceted influences on cells and mitochondria, including calcium handling, autophagy and energetics, as well as the subcellular localization of mitochondrial organelles to neuronal synapses. The remarkable range of physical or functional interactions by Bcl-2 family proteins is challenging to assimilate into a cohesive understanding. Most of their effects may be distinct from their direct roles in apoptotic cell death and are particularly apparent in the nervous system. Dual roles in mitochondrial dynamics and cell death extend beyond BCL-2 family proteins. In this review, we discuss many processes that govern mitochondrial structure and function in health and disease, and how Bcl-2 family proteins integrate into some of these processes.

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“…The only viable way to achieve targeted optical communication in the dense and (seemingly) disordered brain environment is for the photons to travel in waveguides. Mitochondria and microtubules in neurons have been hypothesized to serve as waveguides22232425. However, these structures are too small and inhomogeneous to guide light efficiently over significant distances.…”

mentioning

confidence: 99%

Possible existence of optical communication channels in the brain

Kumar

Boone

Tuszyński

et al. 2016

Sci Rep

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Given that many fundamental questions in neuroscience are still open, it seems pertinent to explore whether the brain might use other physical modalities than the ones that have been discovered so far. In particular it is well established that neurons can emit photons, which prompts the question whether these biophotons could serve as signals between neurons, in addition to the well-known electro-chemical signals. For such communication to be targeted, the photons would need to travel in waveguides. Here we show, based on detailed theoretical modeling, that myelinated axons could serve as photonic waveguides, taking into account realistic optical imperfections. We propose experiments, both in vivo and in vitro, to test our hypothesis. We discuss the implications of our results, including the question whether photons could mediate long-range quantum entanglement in the brain.

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Long range physical cell-to-cell signalling via mitochondria inside membrane nanotubes: a hypothesis

Cited by 38 publications

References 192 publications

Oxidative species-induced excitonic transport in tubulin aromatic networks: Potential implications for neurodegenerative disease

Oxidative species-induced excitonic transport in tubulin aromatic networks: Potential implications for neurodegenerative disease

Connecting mitochondrial dynamics and life-or-death events via Bcl-2 family proteins

Possible existence of optical communication channels in the brain

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