PMID- 22079292
OWN - NLM
STAT- MEDLINE
DCOM- 20120127
LR  - 20211021
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 416
IP  - 1-2
DP  - 2011 Dec 9
TI  - Store-operated calcium entry is present in HL-1 cardiomyocytes and contributes to 
      resting calcium.
PG  - 45-50
LID - 10.1016/j.bbrc.2011.10.133 [doi]
AB  - Store-operated Ca(2+) entry (SOCE) has recently been shown to be of physiological 
      and pathological importance in the heart, particularly during cardiac 
      hypertrophy. However, measuring changes in intracellular Ca(2+) during SOCE is 
      very difficult to study in adult primary cardiomyocytes. As a result there is a 
      need for a stable and reliable in vitro model of SOCE which can be used to test 
      cardiac drugs and investigate the role of SOCE in cardiac pathology. HL-1 cells 
      are the only immortal cardiomyocyte cell line available that continuously divides 
      and spontaneously contracts while maintaining phenotypic characteristics of the 
      adult cardiomyocyte. To date the role of SOCE has not yet been investigated in 
      the HL-1 cardiac cell line. We report for the first time that these cells 
      expressed stromal interaction molecule 1 (STIM1) and the Ca(2+) release-activated 
      Ca(2+) (CRAC) channel Orai1, which are essential components of the SOCE 
      machinery. In addition, SOCE was tightly coupled to sarcoplasmic reticulum 
      (SR)-Ca(2+) release in HL-1 cells, and such response was not impaired in the 
      presence of voltage dependent Ca(2+) channels (L-type and T-type channels) or 
      reverse mode Na(+)/Ca(2+) exchanger (NCX) inhibitors. We were able to abolish the 
      SOCE response with known SOCE inhibitors (BTP-2 and SKF-96365) and by targeted 
      knockdown of Orai1 with RNAi. In addition, knockdown of Orai1 resulted in lower 
      baseline Ca(2+) and an attenuated response to thapsigargin (TG) and caffeine, 
      indicating that SOCE may play a role in Ca(2+) homeostasis during unstressed 
      conditions in cardiomyocytes. Currently, there is little knowledge about SOCE in 
      cardiomyocytes, and the present results suggest that HL-1 cells will be of great 
      utility in investigating the role of SOCE in the heart.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Touchberry, Chad D
AU  - Touchberry CD
AD  - School of Medicine, Muscle Biology Research Group, University of Missouri-Kansas 
      City, Kansas City, MO 64108, USA.
FAU - Elmore, Chris J
AU  - Elmore CJ
FAU - Nguyen, Tien M
AU  - Nguyen TM
FAU - Andresen, Jon J
AU  - Andresen JJ
FAU - Zhao, Xiaoli
AU  - Zhao X
FAU - Orange, Matthew
AU  - Orange M
FAU - Weisleder, Noah
AU  - Weisleder N
FAU - Brotto, Marco
AU  - Brotto M
FAU - Claycomb, William C
AU  - Claycomb WC
FAU - Wacker, Michael J
AU  - Wacker MJ
LA  - eng
GR  - R00 AR054793-03/AR/NIAMS NIH HHS/United States
GR  - R00 AR054793-04/AR/NIAMS NIH HHS/United States
GR  - R21 HL076498-02/HL/NHLBI NIH HHS/United States
GR  - R00 AR054793/AR/NIAMS NIH HHS/United States
GR  - AR054793/AR/NIAMS NIH HHS/United States
GR  - R21 HL076498/HL/NHLBI NIH HHS/United States
GR  - K99 AR054793/AR/NIAMS NIH HHS/United States
GR  - HL076498/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20111106
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Calcium Channels)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (ORAI1 Protein)
RN  - 0 (Orai1 protein, mouse)
RN  - 0 (Stim1 protein, mouse)
RN  - 0 (Stromal Interaction Molecule 1)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channels/genetics/metabolism
MH  - Cell Line
MH  - Gene Knockdown Techniques
MH  - Homeostasis
MH  - Membrane Glycoproteins/genetics/metabolism
MH  - Mice
MH  - *Models, Biological
MH  - Myocytes, Cardiac/*metabolism
MH  - ORAI1 Protein
MH  - Stromal Interaction Molecule 1
PMC - PMC3237803
MID - NIHMS336941
EDAT- 2011/11/15 06:00
MHDA- 2012/01/28 06:00
PMCR- 2012/12/09
CRDT- 2011/11/15 06:00
PHST- 2011/10/27 00:00 [received]
PHST- 2011/10/27 00:00 [accepted]
PHST- 2011/11/15 06:00 [entrez]
PHST- 2011/11/15 06:00 [pubmed]
PHST- 2012/01/28 06:00 [medline]
PHST- 2012/12/09 00:00 [pmc-release]
AID - S0006-291X(11)01967-X [pii]
AID - 10.1016/j.bbrc.2011.10.133 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2011 Dec 9;416(1-2):45-50. doi: 
      10.1016/j.bbrc.2011.10.133. Epub 2011 Nov 6.