Mitochondrial channels revisited

1996 ◽  
Vol 28 (2) ◽  
pp. 89-91 ◽  
Author(s):  
Carmen A. Mannella
Keyword(s):  
Mitochondrial Channels

Mitochondrial Channels

2004 ◽  
pp. 689-692
Author(s):  
M. Catia Sorgato ◽  
Alessandro Bertoli
Keyword(s):  
Mitochondrial Channels

Mitochondrial Channels Permeable by Calcium Ions

2004 ◽  
Vol 14 (1-2) ◽  
pp. 35-39 ◽  
Author(s):  
Viera Komínková ◽  
Marta Novotová ◽  
Karol Ondriaš ◽  
Tatiana Ravingerová ◽  
Adam Szewczyk
Keyword(s):  
Calcium Ions ◽  
Mitochondrial Channels

Differential staining of crystalline arrays of outer mitochondrial membrane channels

1983 ◽  
Vol 41 ◽  
pp. 444-445
Author(s):  
Carmen A. Mannella ◽  
Joachim Frank
Keyword(s):  
Mitochondrial Membrane ◽  
Differential Staining ◽  
Mitochondrial Outer Membrane ◽  
Outer Mitochondrial Membrane ◽  
Mitochondrial Channels ◽  
Outer Membranes ◽  
Main Protein ◽  
Protein Components ◽  
Regular Arrays

The mitochondrial outer membrane contains pore-forming polypeptides (Mr⋍= 30,000) which are its main protein components in plants and fungi. Outer membranes (OM) isolated from Neurospora mitochondria often contain extended regular arrays of subunits with stain-accumulating centers 2-3 nm in diameter. That these subunits are the mitochondrial channels has been established immunologically. Antibodies against the predominant 31-kDa OM polypeptide of Neurospora (a) prevent in vitro insertion of OM channels into bilayers and (b) preferentially bind to the crystalline membranes in OM fractions.Planar projections of individual OM channel layers have been reconstructed from electron micrographs of negatively stained crystalline vesicles by Fourier filtration. In the usual array (Fig. 1a) the unit cell is a parallelogram which can hold six stain centers (putative pore openings) arranged in a hexagon with p2 symmetry. There are large pore-free areas in these arrays (* in Fig. 1a) which are likely composed of phospholipid, since they disappear when the membranes are treated with phospholipase A2 (Fig. 1b).

Electrophysiological Studies of Mitochondrial Channels

Neurobiology ◽  
1996 ◽  
pp. 11-21
Author(s):  
Maria Luisa Campo ◽  
Concepción Muro ◽  
Henry Tedeschi ◽  
Kathleen W. Kinnally
Keyword(s):  
Mitochondrial Channels ◽  
Electrophysiological Studies

Po2 cycling protects diaphragm function during reoxygenation via ROS, Akt, ERK, and mitochondrial channels

2015 ◽  
Vol 309 (11) ◽  
pp. C759-C766 ◽  
Author(s):  
Li Zuo ◽  
Benjamin K. Pannell ◽  
Anthony T. Re ◽  
Thomas M. Best ◽  
Peter D. Wagner
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Low Oxygen ◽  
Mitochondrial Channels ◽  
Extracellular Signal Regulated Kinase ◽  
Cycling Treatment ◽  
Extracellular Signal

Po2 cycling, often referred to as intermittent hypoxia, involves exposing tissues to brief cycles of low oxygen environments immediately followed by hyperoxic conditions. After experiencing long-term hypoxia, muscle can be damaged during the subsequent reintroduction of oxygen, which leads to muscle dysfunction via reperfusion injury. The protective effect and mechanism behind Po2 cycling in skeletal muscle during reoxygenation have yet to be fully elucidated. We hypothesize that Po2 cycling effectively increases muscle fatigue resistance through reactive oxygen species (ROS), protein kinase B (Akt), extracellular signal-regulated kinase (ERK), and certain mitochondrial channels during reoxygenation. Using a dihydrofluorescein fluorescent probe, we detected the production of ROS in mouse diaphragmatic skeletal muscle in real time under confocal microscopy. Muscles treated with Po2 cycling displayed significantly attenuated ROS levels ( n = 5; P < 0.001) as well as enhanced force generation compared with controls during reperfusion ( n = 7; P < 0.05). We also used inhibitors for signaling molecules or membrane channels such as ROS, Akt, ERK, as well as chemical stimulators to close mitochondrial ATP-sensitive potassium channel (KATP) or open mitochondrial permeability transition pore (mPTP). All these blockers or stimulators abolished improved muscle function with Po2 cycling treatment. This current investigation has discovered a correlation between KATP and mPTP and the Po2 cycling pathway in diaphragmatic skeletal muscle. Thus we have identified a unique signaling pathway that may involve ROS, Akt, ERK, and mitochondrial channels responsible for Po2 cycling protection during reoxygenation conditions in the diaphragm.

Ionic mitochondrial channels: characteristics and possible role in protein translocation

Biochimie ◽  
1989 ◽  
Vol 71 (8) ◽  
pp. 963-968 ◽  
Author(s):  
Jean-Pierre Henry ◽  
Jean-François Chich ◽  
Denise Goldschmidt ◽  
Michel Thieffry
Keyword(s):  
Protein Translocation ◽  
Mitochondrial Channels

scholarly journals Mitochondrial Channels and their Role in Cardioprotection

2021 ◽  
Author(s):  
Keerti Mishra ◽  
Min Luo
Keyword(s):  
Heart Failure ◽  
Potassium Channels ◽  
Ischemic Preconditioning ◽  
Current Knowledge ◽  
Pivotal Role ◽  
Mitochondrial Channels ◽  
Development Therapy ◽  
Ischemic Episode ◽  
Calcium Activated Potassium Channels ◽  
End Effectors

Mitochondria play a pivotal role in cardioprotection. The major cardioprotective mechanism is ischemic preconditioning (IpreC), through which short periods of ischemia protect a subsequent prolonged acute ischemic episode. Mitochondria channels, particularly the potassium channels (mitoK) such as ATP-dependent and calcium-activated potassium channels, have been suggested as trigger or end effectors in IpreC. Activators of mitoK are promising therapeutic agents for the treatment of the myocardial injury due to ischemic episodes. In this chapter, we are summarizing our current knowledge on the physiology function of different mitochondrial channels with a focus on the potassium channels and their mechanism in cardioprotection. Furthermore, the currently under development therapy by targeting the mitochondrial channels for the treatment of heart failure are also discussed.

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