Characterization of Myelin Sheath FoF1-ATP Synthase and its Regulation by IF1

Ravera, Silvia; Panfoli, Isabella; Aluigi, Maria Grazia; Calzia, Daniela; Morelli, Alessandro

doi:10.1007/s12013-010-9112-1

Cited by 46 publications

(52 citation statements)

References 46 publications

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“…Moreover, we explored the possibility that oligodendrocyte support of the axon involves energy metabolism. The latter hypothesis has been recently proposed by some of us [16] and stems among else (1) from previous research by some of us [22,23] showing that the myelin sheath is capable of aerobic metabolism and ATP synthesis and (2) from the consideration that damage to the oligodendrocytes not only slows down conduction velocity, but also causes a morphological degeneration of the axons they wrap [6]. The latter finding strongly suggests that myelin provides some form of metabolic support to the axons, the nature of which has not been elucidated yet.…”

Section: Introductionmentioning

confidence: 80%

“…Some of us previously showed that myelin vescicles contain functional FoF1-ATP synthase and respiratory chain complexes and are able to conduct aerobic metabolism [22,23].…”

Section: Discussionmentioning

confidence: 99%

“…Some of us recently found that myelin from mammalian brain or optic nerve perform aerobic ATP synthesis [22,23]. Given the above mentioned considerations, this finding prompted us to hypothesize that the glial-axonal interaction may involve the transfer of ATP from the myelin sheath to the axon [16].…”

Section: Introductionmentioning

confidence: 99%

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A Novel Hypothesis About Mechanisms Affecting Conduction Velocity of Central Myelinated Fibers

et al. 2011

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The hypothesis that gap junctions are implicated in facilitating axonal conduction has not yet been experimentally demonstrated at the electrophysiological level. We found that block of gap junctions with oleammide slows down axonal conduction velocity in the hippocampal Schaffer collaterals, a central myelinated pathway. Moreover, we explored the possibility that support by the oligodendrocyte to the axon involves energy metabolism, a hypothesis that has been recently proposed by some of us. In agreement with this hypothesis, we found that the effect of oleammide was reversed by pretreatment with creatine, a compound that is known to increase the energy charge of the tissue. Moreover, conduction velocity was also slowed down by anoxia, a treatment that obviously decreases the energy charge of the tissue, and by ouabain, a compound that blocks plasma membrane Na/K-ATPase, the main user of ATP in the brain. We hypothesize that block of gap junctions slows down conduction velocity in central myelinated pathways because oligodendrocytes synthesize ATP and transfer it to the axon through gap junctions.

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Section: Introductionmentioning

confidence: 80%

“…Some of us previously showed that myelin vescicles contain functional FoF1-ATP synthase and respiratory chain complexes and are able to conduct aerobic metabolism [22,23].…”

Section: Discussionmentioning

confidence: 99%

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A Novel Hypothesis About Mechanisms Affecting Conduction Velocity of Central Myelinated Fibers

et al. 2011

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“…We have previously reported the functional ectopic expression of ATP synthase and ETC on mammalian retinal rod outer segments disks and bovine brain IMV coupled to a consistent aerobic ATP production (in the micromolar range) which we hypothesized to supply the energetic demands of these two high energy requiring tissues, that are devoid of mitochondria (Panfoli et al 2008;Ravera et al 2009;2010). In hepatome cells, ATP synthase was hypothesised to control the extracellular ADP/ ATP ratio, and intracellular pH homeostasis (Mangiullo et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Evidence for Ectopic Aerobic ATP Production on C6 Glioma Cell Plasma Membrane

et al. 2010

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Extracellular ATP plays a pivotal role as a signaling molecule in physiological and pathological conditions in the CNS. In several glioma cell lines, ATP is a positive factor for one or more characteristics important for the abnormal growth and survival of these cells. This work presents immunofluorescence and biochemical analyses suggesting that an aerobic metabolism, besides mitochondria, is located also on the plasma membrane of C6 glioma cells. An ATP synthesis coupled to oxygen consumption was measured in plasma membrane isolated from C6 cells, sensitive to common inhibitors of respiratory chain complexes, suggesting the involvement of a putative surface ATP synthase complex. Immunofluorescence imaging showed that Cytochrome c oxydase colocalized with WGA, a typical plasma membrane protein, on the plasma membrane of glioma cells. Cytochrome c oxydase staining pattern appeared punctuate, suggesting the intriguing possibility that the redox chains may be expressed in discrete sites on C6 glioma cell membrane. Data suggest that the whole respiratory chain is localized on C6 glioma cell surface. Moreover, when resveratrol, an ATP synthase inhibitor, was added to culture medium, a cytostatic effect was observed, suggesting a correlation among the ectopic ATP synthesis and the tumor growth. So, a potential direction for the design of new targets for future therapies may arise.

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“…This has generated an interesting dispute [36,37] about the implications of myelin ability to aerobically synthesize ATP, both in CNS [38][39][40] and PNS [41], with a pivotal role of connexins [42].…”

Section: Evaluation Of the Hypothesismentioning

confidence: 99%

Why do premature newborn infants display elevated blood adenosine levels?

et al. 2016

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Link to publicationCitation for published version (APA): Panfoli, I., Cassanello, M., Bruschettini, M., Colella, M., Cerone, R., Ravera, S., ... Ramenghi, L. (2016). Why do premature newborn infants display elevated blood adenosine levels ? Medical Hypotheses, 90, 53-56. DOI: 10.1016/j.mehy.2016 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Take down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. WHY DO PREMATURE NEWBORN INFANTS DISPLAY ELEVATED BLOOD ADENOSINE LEVELS?Isabella ABSTRACTOur preliminary data show high levels of adenosine in the blood of very low birth weight (VLBW) infants, positively correlating to their prematurity (i.e. body weight class). This prompted us to look for a mechanism promoting such impressive adenosine increase. We hypothesized a correlation with oxygen challenge. In fact, it is recognized that either oxygen lack or its excess contribute to the pathogenesis of the injuries of prematurity, such as retinopathy (ROP) and periventricular white matter lesions (PWMI). The optimal concentration of oxygen for resuscitation of VLBW infants is currently under revision.We propose that the elevated adenosine blood concentrations of VLBW infants recognizes two sources. The first could be its activity-dependent release from unmyelinated brain axons.

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Characterization of Myelin Sheath FoF1-ATP Synthase and its Regulation by IF1

Cited by 46 publications

References 46 publications

A Novel Hypothesis About Mechanisms Affecting Conduction Velocity of Central Myelinated Fibers

A Novel Hypothesis About Mechanisms Affecting Conduction Velocity of Central Myelinated Fibers

Evidence for Ectopic Aerobic ATP Production on C6 Glioma Cell Plasma Membrane

Why do premature newborn infants display elevated blood adenosine levels?

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