Mitochondrial Membrane Potential Probes and the Proton Gradient: A Practical Usage Guide

Perry, Seth W.; Norman, John P.; Barbieri, Justin; Brown, Edward B.; Gelbard, Harris A.

doi:10.2144/000113610

Cited by 971 publications

(837 citation statements)

References 73 publications

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“…Together with the mitochondrial localization, this suggested that PPAN might act at the level of mitochondrial apoptosis. To test this, we monitored MOMP by use of MitoTracker, which is a well known readout for this purpose (39,40). Indeed, siRNA-mediated knockdown of PPAN resulted in a greatly reduced signal for MitoTracker thereby indicating loss of mitochondrial membrane potential and increase of MOMP (Fig.…”

Section: Ppan Is Released From Nucleoli and Cleaved After Acd Treatmementioning

confidence: 99%

The Wnt Target Protein Peter Pan Defines a Novel p53-independent Nucleolar Stress-Response Pathway

Pfister

Keil

Kühl

2015

Journal of Biological Chemistry

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Background: Peter Pan (PPAN) localizes to nucleoli and functions in ribosome biogenesis. Results: PPAN localizes also to mitochondria, and PPAN knockdown triggers p53-independent mitochondrial apoptosis and nucleolar stress as observed by de-stabilization of nucleophosmin. Conclusion: PPAN orchestrates a p53-independent stress-response pathway by coupling nucleolar stress induction to the mitochondrial apoptosis. Significance: Novel insight into the anti-apoptotic role of the ribosome processing factor PPAN is provided.

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Section: Ppan Is Released From Nucleoli and Cleaved After Acd Treatmementioning

confidence: 99%

The Wnt Target Protein Peter Pan Defines a Novel p53-independent Nucleolar Stress-Response Pathway

Pfister

Keil

Kühl

2015

Journal of Biological Chemistry

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“…Mitochondrial membrane potential is often considered a measure of mitochondrial functionality, since a higher membrane potential may support a larger respiratory rate and ATP/ADP ratio [27,28], as well as its role in quality control [20] (although this correspondence may not hold under all conditions, since inhibiting ATP synthase can cause membrane potential to increase [28,29]). It is important to distinguish between total DC, which is expected to scale with a characteristic size of the system (e.g.…”

Section: Linking Mitochondrial Heterogeneity and Cell Sizementioning

confidence: 99%

Mitochondrial heterogeneity, metabolic scaling and cell death

et al. 2017

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Heterogeneity in mitochondrial content has been previously suggested as a major contributor to cellular noise, with multiple studies indicating its direct involvement in biomedically important cellular phenomena. A recently published dataset explored the connection between mitochondrial functionality and cell physiology, where a non-linearity between mitochondrial functionality and cell size was found. Using mathematical models, we suggest that a combination of metabolic scaling and a simple model of cell death may account for these observations. However, our findings also suggest the existence of alternative competing hypotheses, such as a non-linearity between cell death and cell size. While we find that the proposed non-linear coupling between mitochondrial functionality and cell size provides a compelling alternative to previous attempts to link mitochondrial heterogeneity and cell physiology, we emphasise the need to account for alternative causal variables, including cell cycle, size, mitochondrial density and death, in future studies of mitochondrial physiology.

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“…This oxygenation leads to the first stage of cellular respiration, glycolysis. Protons from the high-energy bonds of NADH and FADH 2 that are pumped across the mitochondrial membrane [59] lead to membrane hyperpolarization [60], in which the interior matrix voltage of the mitochondria is more negative [61]. At the same time, during inhalation, the inflation of alveoli and the trancheo-bronchial tree may cause SARs to send hyperpolarization impulses to the brain [47].…”

Section: Influence Of Respiration On the Cellular Levelmentioning

confidence: 99%

Widespread depolarization during expiration: A source of respiratory drive?

Jerath¹,

Crawford²,

Barnes

et al. 2015

Medical Hypotheses

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a b s t r a c tRespiration influences various pacemakers and rhythms of the body during inspiration and expiration but the underlying mechanisms are relatively unknown. Understanding this phenomenon is important, as breathing disorders, breath holding, and hyperventilation can lead to significant medical conditions. We discuss the physiological modulation of heart rhythm, blood pressure, sympathetic nerve activity, EEG, and other changes observed during inspiration and expiration. We also correlate the intracellular mitochondrial respiratory metabolic processes with real-time breathing and correlate membrane potential changes with inspiration and expiration. We propose that widespread minor hyperpolarization occurs during inspiration and widespread minor depolarization occurs during expiration. This depolarization is likely a source of respiratory drive. Further knowledge of intracellular and extracellular ionic changes associated with respiration will enhance our understanding of respiration and its role as a modulator of cellular membrane potential. This could expand treatment options for a wide range of health conditions, such as breathing disorders, stress-related disorders, and further our understanding of the Hering-Breuer reflex and respiratory sinus arrhythmia.Ó 2014 Elsevier Ltd. All rights reserved. IntroductionIn addition to gas exchange and oxygenation of the blood, respiration in the lungs can regulate multiple physiological processes throughout the body. Studies of the cardiovascular system, the peripheral nervous system, and the central nervous system provide evidence that respiratory patterns can exert a significant and immediate influence on a wide range of bodily functions, including changes in blood pressure and sympathovagal balance. Patterned respiration can regulate blood pressure and heart rate [1], as well as regulate rhythmic centers of the brain that control cardiovascular output [2,3]. While the majority of these findings have demonstrated the impact of respiration on cardiac output and other processes in isolated preparations, little work has focused on respiration's direct influence on membrane potential.This article reviews the current understanding of respiration as a regulator of cardiovascular physiology and nervous system function. More specifically, we discuss the role of respiratory rhythm and rate on both systemic and local control of these systems. We describe the role of pulmonary stretch receptors (with a focus on slowly adapting receptors) in converting breathing patterns into a functional, multi-faceted, mechanism that allows respiration to communicate with, and direct various aspects of cardiovascular and nervous system physiology. We propose a hypothesis in which inspiration and expiration are associated with transient increases and decreases in membrane potential that may underlie these widespread changes and how these membrane potential changes may underlie the chaotic dynamics of rhythmic breathing.Many studies focus on the brainstem as the primary modulator of resp...

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Mitochondrial Membrane Potential Probes and the Proton Gradient: A Practical Usage Guide

Cited by 971 publications

References 73 publications

The Wnt Target Protein Peter Pan Defines a Novel p53-independent Nucleolar Stress-Response Pathway

The Wnt Target Protein Peter Pan Defines a Novel p53-independent Nucleolar Stress-Response Pathway

Mitochondrial heterogeneity, metabolic scaling and cell death

Widespread depolarization during expiration: A source of respiratory drive?

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