scholarly journals Role of BK Channels in the Apoptotic Volume Decrease in Native Eel Intestinal Cells

2010 ◽  
Vol 25 (6) ◽  
pp. 733-744 ◽  
Author(s):  
Maria Giulia Lionetto ◽  
Maria Elena Giordano ◽  
Antonio Calisi ◽  
Roberto Caricato ◽  
Else Hoffmann ◽  
...  
Keyword(s):  
Bk Channels ◽  
Intestinal Cells ◽  
Apoptotic Volume Decrease ◽  
Volume Decrease

scholarly journals Role of TASK2 in the Control of Apoptotic Volume Decrease in Proximal Kidney Cells

2007 ◽  
Vol 282 (50) ◽  
pp. 36692-36703 ◽  
Author(s):  
Sébastien L'Hoste ◽  
Mallorie Poet ◽  
Christophe Duranton ◽  
Radia Belfodil ◽  
Herv é Barriere ◽  
...  
Keyword(s):  
Kidney Cells ◽  
Apoptotic Volume Decrease ◽  
Volume Decrease

scholarly journals Differential role of IK and BK potassium channels as mediators of intrinsic and extrinsic apoptotic cell death

2012 ◽  
Vol 303 (10) ◽  
pp. C1070-C1078 ◽  
Author(s):  
Michael B. McFerrin ◽  
Kathryn L. Turner ◽  
Vishnu Anand Cuddapah ◽  
Harald Sontheimer
Keyword(s):  
Cell Volume ◽  
Apoptotic Cell ◽  
Bk Channels ◽  
Bk Channel ◽  
Extrinsic Pathway ◽  
Tnf Α ◽  
Dependent Cell ◽  
Necessary And Sufficient ◽  
Volume Decrease

An important event during apoptosis is regulated cell condensation known as apoptotic volume decrease (AVD). Ion channels have emerged as essential regulators of this process mediating the release of K+ and Cl−, which together with osmotically obliged water, results in the condensation of cell volume. Using a Grade IV human glioblastoma cell line, we examined the contribution of calcium-activated K+ channels (KCa channels) to AVD after the addition of either staurosporine (Stsp) or TNF-α-related apoptosis-inducing ligand (TRAIL) to activate the intrinsic or extrinsic pathway of apoptosis, respectively. We show that AVD can be inhibited in both pathways by high extracellular K+ or the removal of calcium. However, BAPTA-AM was only able to inhibit Stsp-initiated AVD, whereas TRAIL-induced AVD was unaffected. Specific KCa channel inhibitors revealed that Stsp-induced AVD was dependent on K+ efflux through intermediate-conductance calcium-activated potassium (IK) channels, while TRAIL-induced AVD was mediated by large-conductance calcium-activated potassium (BK) channels. Fura-2 imaging demonstrated that Stsp induced a rapid and modest rise in calcium that was sustained over the course of AVD, while TRAIL produced no detectable rise in global intracellular calcium. Inhibition of IK channels with clotrimazole or 1-[(2-chlorophenyl) diphenylmethyl]-1 H-pyrazole (TRAM-34) blocked downstream caspase-3 activation after Stsp addition, while paxilline, a specific BK channel inhibitor, had no effect. Treatment with ionomycin also induced an IK-dependent cell volume decrease. Together these results show that calcium is both necessary and sufficient to achieve volume decrease and that the two major pathways of apoptosis use unique calcium signaling to efflux K+ through different KCa channels.

Staurosporine-induced cell death in salmonid cells: the role of apoptotic volume decrease, ion fluxes and MAP kinase signaling

APOPTOSIS ◽  
2007 ◽  
Vol 12 (10) ◽  
pp. 1755-1768 ◽  
Author(s):  
Gerhard Krumschnabel ◽  
Tanja Maehr ◽  
Muhammad Nawaz ◽  
Pablo J. Schwarzbaum ◽  
Claudia Manzl
Keyword(s):  
Cell Death ◽  
Map Kinase ◽  
Ion Fluxes ◽  
Kinase Signaling ◽  
Apoptotic Volume Decrease ◽  
Map Kinase Signaling ◽  
Volume Decrease

The Yin and Yang of BK Channels in Epilepsy

2018 ◽  
Vol 17 (4) ◽  
pp. 272-279 ◽  
Author(s):  
Yudan Zhu ◽  
Shuzhang Zhang ◽  
Yijun Feng ◽  
Qian Xiao ◽  
Jiwei Cheng ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Bk Channels ◽  
Bk Channel ◽  
Potential Shape ◽  
Yin And Yang ◽  
The Central Nervous System ◽  
Action Potential Shape ◽  
Excitability Of Neurons

Background & Objective: The large conductance calcium-activated potassium (BK) channel, extensively distributed in the central nervous system (CNS), is considered as a vital player in the pathogenesis of epilepsy, with evidence implicating derangement of K+ as well as regulating action potential shape and duration. However, unlike other channels implicated in epilepsy whose function in neurons could clearly be labeled “excitatory” or “inhibitory”, the unique physiological behavior of the BK channel allows it to both augment and decrease the excitability of neurons. Thus, the role of BK in epilepsy is controversial so far, and a growing area of intense investigation. Conclusion: Here, this review aims to highlight recent discoveries on the dichotomous role of BK channels in epilepsy, focusing on relevant BK-dependent pro- as well as antiepileptic pathways, and discuss the potential of BK specific modulators for the treatment of epilepsy.

Volume changes in the legs of paraplegic subjects during arm exercise

1993 ◽  
Vol 75 (5) ◽  
pp. 2079-2083 ◽  
Author(s):  
M. T. Hopman ◽  
P. H. Verheijen ◽  
R. A. Binkhorst
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Lesion ◽  
Volume Changes ◽  
Arm Exercise ◽  
Cord Injury ◽  
Exercise Period ◽  
Exercise Muscle ◽  
Cord Lesion ◽  
Volume Decrease

The purpose of this study was to examine the inability of paraplegic (P) subjects to redistribute fluid below the spinal cord lesion during arm exercise, with emphasis on the role of the sympathetic system in this redistribution failure. Fifteen male P and 15 male able-bodied [control (C)] subjects performed arm cranking exercise, and volume changes in the calf were measured by strain gauge plethysmography before, during, and after exercise. Muscle pump activity in the legs of C subjects was eliminated. The rate of calf volume decrease at the beginning and halfway points of the exercise period, the total volume decrease during exercise, and the volume increase during recovery were significantly lower in P than in C subjects. Whereas completeness of the lesion had no influence on leg volume changes, the rate of calf volume decrease at the beginning of exercise and the total volume decrease during exercise were significantly correlated with the level of the spinal cord lesion. This study confirms that P subjects are unable to redistribute fluid effectively below the spinal cord injury during arm exercise, which is partly caused by a loss of sympathetically induced vasoconstriction and which appears to be independent of the completeness of the lesion but dependent on its level.

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