PMID- 21241999
OWN - NLM
STAT- MEDLINE
DCOM- 20110610
LR  - 20131121
IS  - 1532-1991 (Electronic)
IS  - 0143-4160 (Linking)
VI  - 49
IP  - 2
DP  - 2011 Feb
TI  - Voltage-dependent anion channel 2 modulates resting Ca(2)+ sparks, but not action 
      potential-induced Ca(2)+ signaling in cardiac myocytes.
PG  - 136-43
LID - 10.1016/j.ceca.2010.12.004 [doi]
AB  - Voltage-dependent anion channels (VDACs) are pore forming proteins predominantly 
      found in the outer mitochondrial membrane and are thought to transport Ca(2+). In 
      this study, we have investigated the possible role of type 2 VDAC (VDAC2) in 
      cardiac Ca(2+) signaling and Ca(2+) sparks using a lentiviral knock-down (KD) 
      technique and two-dimensional confocal Ca(2+) imaging in immortalized 
      autorhythmic adult atrial cells, HL-1. We confirmed high expression of VDAC2 
      protein in ventricular, atrial, and HL-1 cells using Western blot analysis. 
      Infection of HL-1 cells with VDAC2-targeting lentivirus reduced the level of 
      VDAC2 protein to  approximately 10%. Comparisons of autorhythmic Ca(2+) transients between 
      wild-type (WT) and VDAC2 KD cells showed no significant change in the magnitude, 
      decay, and beating rate of the Ca(2+) transients. Caffeine (10mM)-induced Ca(2+) 
      release, which indicates sarcoplasmic reticulum (SR) Ca(2+) content, was not 
      altered by VDAC2 KD. Interestingly, however, the intensity, width, and duration 
      of the individual Ca(2+) sparks were significantly increased by VDAC2 KD in 
      resting conditions, with no change in the frequency of sparks. VDAC2 KD 
      significantly delayed mitochondrial Ca(2+) uptake during artificial Ca(2+) pulses 
      in permeabilized HL-1 cells. These results suggest that VDAC2 may facilitate 
      mitochondrial Ca(2+) uptake and restrict Ca(2+) spark expansion without 
      regulating activations of sparks under resting conditions, thereby providing 
      evidence on the functional role of VDAC2 in cardiac local Ca(2+) signaling.
CI  - Copyright (c) 2010 Elsevier Ltd. All rights reserved.
FAU - Subedi, Krishna Prasad
AU  - Subedi KP
AD  - College of Pharmacy, IDRD, Chungnam National University, 220 Gung-dong, 
      Yuseong-gu, Daejeon 305-764, South Korea.
FAU - Kim, Joon-Chul
AU  - Kim JC
FAU - Kang, Moonkyung
AU  - Kang M
FAU - Son, Min-Jeong
AU  - Son MJ
FAU - Kim, Yeon-Soo
AU  - Kim YS
FAU - Woo, Sun-Hee
AU  - Woo SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110115
PL  - Netherlands
TA  - Cell Calcium
JT  - Cell calcium
JID - 8006226
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Voltage-Dependent Anion Channel 2)
RN  - 3G6A5W338E (Caffeine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Action Potentials
MH  - Animals
MH  - Caffeine/pharmacology
MH  - Calcium/*metabolism
MH  - Calcium Signaling/*physiology
MH  - Cell Line, Transformed
MH  - Mice
MH  - Myocytes, Cardiac/cytology/*metabolism
MH  - RNA Interference
MH  - RNA, Small Interfering/metabolism
MH  - Sarcoplasmic Reticulum/metabolism
MH  - Voltage-Dependent Anion Channel 2/genetics/*metabolism
EDAT- 2011/01/19 06:00
MHDA- 2011/06/11 06:00
CRDT- 2011/01/19 06:00
PHST- 2010/07/29 00:00 [received]
PHST- 2010/11/12 00:00 [revised]
PHST- 2010/12/20 00:00 [accepted]
PHST- 2011/01/19 06:00 [entrez]
PHST- 2011/01/19 06:00 [pubmed]
PHST- 2011/06/11 06:00 [medline]
AID - S0143-4160(10)00205-8 [pii]
AID - 10.1016/j.ceca.2010.12.004 [doi]
PST - ppublish
SO  - Cell Calcium. 2011 Feb;49(2):136-43. doi: 10.1016/j.ceca.2010.12.004. Epub 2011 
      Jan 15.