Voltage-dependent anion channels: their roles in plant defense and cell death

AbstractThe purpose of this study was to investigate the role of voltage-dependent anion channel (VDAC) in mitochondria-mediated apoptosis of neurons in refractory epilepsy. Western blot analyses were carried out to detect the changes in cytochrome C, caspase 9, Bax, and Bcl-2. TUNEL assays were also carried out to investigate cell apoptosis under the upregulation and downregulation of VDAC1 with or without Bax or Bcl-2. VDAC1 induced Bax, Bcl-2, and caspase 9, increasing the release of cytochrome C. VDAC1 played an essential role in the apoptotic cell death of refractory epilepsy. It is concluded that VDAC1 plays an important role in refractory epilepsy and could be a possible therapeutic target of anti-epileptic drugs. The current study provides a new understanding of the possible mechanisms of refractory epilepsy.

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Faculty Opinions recommendation of Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1079779.535901 ◽

2007 ◽

Author(s):

Terrence Frey

Keyword(s):

Cell Death ◽

Anion Channels ◽

Voltage Dependent ◽

Dependent Cell

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RAS–RAF–MEK-dependent oxidative cell death involving voltage-dependent anion channels

Nature ◽

10.1038/nature05859 ◽

2007 ◽

Vol 447 (7146) ◽

pp. 865-869 ◽

Cited By ~ 426

Author(s):

Nicholas Yagoda ◽

Moritz von Rechenberg ◽

Elma Zaganjor ◽

Andras J. Bauer ◽

Wan Seok Yang ◽

...

Keyword(s):

Cell Death ◽

Anion Channels ◽

Voltage Dependent

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Plant voltage-dependent anion channels are involved in host defense against Pseudomonas cichorii and in Bax-induced cell death

Plant Cell Reports ◽

10.1007/s00299-008-0630-x ◽

2008 ◽

Vol 28 (1) ◽

pp. 41-51 ◽

Cited By ~ 26

Author(s):

Chika Tateda ◽

Koji Yamashita ◽

Fumio Takahashi ◽

Tomonobu Kusano ◽

Yoshihiro Takahashi

Keyword(s):

Cell Death ◽

Host Defense ◽

Anion Channels ◽

Pseudomonas Cichorii ◽

Voltage Dependent

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Voltage-dependent block of endothelial volume-regulated anion channels by calix[4]arenes

AJP Cell Physiology ◽

10.1152/ajpcell.1998.275.3.c646 ◽

1998 ◽

Vol 275 (3) ◽

pp. C646-C652 ◽

Cited By ~ 34

Author(s):

Guy Droogmans ◽

Jean Prenen ◽

Jan Eggermont ◽

Thomas Voets ◽

Bernd Nilius

Keyword(s):

Open Channel ◽

Single Channel ◽

Anion Channel ◽

Anion Channels ◽

Channel Conductance ◽

Open Channel Block ◽

Maximum Inhibition ◽

Voltage Dependent ◽

A Site ◽

Maximal Block

We have studied the effects of calix[4]arenes on the volume-regulated anion channel (VRAC) currents in cultured calf pulmonary artery endothelial cells. TS- and TS-TM-calix[4]arenes induced a fast inhibition at positive potentials but were ineffective at negative potentials. Maximal block occurred at potentials between 30 and 50 mV. Lowering extracellular pH enhanced the block and shifted the maximum inhibition to more negative potentials. Current inhibition was also accompanied by an increased current noise. From the analysis of the calix[4]arene-induced noise, we obtained a single-channel conductance of 9.3 ± 2.1 pS ( n = 9) at +30 mV. The voltage- and time-dependent block were described using a model in which calix[4]arenes bind to a site at an electrical distance of 0.25 inside the channel with an affinity of 220 μM at 0 mV. Binding occludes VRAC at moderately positive potentials, but calix[4]arenes permeate the channel at more positive potentials. In conclusion, our data suggest an open-channel block of VRAC by calix[4]arenes that also depends on the protonation of the binding site within the pore.

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