The question of whether the activation of SOCs (store-operated Ca2+ channels) requires the whole or part of the ER (endoplasmic reticulum) has not been fully resolved. The role of a putative sub-compartment of the ER in SOC activation in liver cells was investigated using ectopically expressed TRPV1 (transient receptor potential vanilloid 1), a non-selective cation channel, and TDCA (taurodeoxycholic acid), an activator of SOCs, to release Ca2+ from different regions of the ER. TRPV1 was expressed in the ER and in the plasma membrane. The amount of Ca2+ released from the ER by a TRPV1 agonist, measured using fura-2, was the same as that released by a SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase) inhibitor, indicating that TRPV1 agonist-sensitive stores substantially overlap with SERCA inhibitor-sensitive stores. In contrast with SERCA inhibitors, TRPV1 agonists did not activate store-operated Ca2+ entry. These findings were confirmed by patch-clamp recording. Using FFP-18, it was shown that SERCA inhibitors release Ca2+ from the ER located closer to the plasma membrane than the region from which TRPV1 agonists release Ca2+. In contrast with SERCA inhibitors, TRPV1 agonists did not induce a redistribution of STIM1 (stromal interaction molecule 1). TDCA caused the release of Ca2+ from the ER, which was detected by FFP-18 but not by fura-2, and a redistribution of STIM1 to puncta similar to that caused by SERCA inhibitors. It is concluded that in liver cells, Ca2+ release from a small component of the ER located near the plasma membrane is required to induce STIM1 redistribution and SOC activation.
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Research Article|
February 25 2009
A small component of the endoplasmic reticulum is required for store-operated Ca2+ channel activation in liver cells: evidence from studies using TRPV1 and taurodeoxycholic acid
Joel Castro;
Joel Castro
*Department of Medical Biochemistry, School of Medicine, Flinders University, Adelaide, South Australia 5001, Australia
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Edoardo C. Aromataris;
Edoardo C. Aromataris
†School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia
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Grigori Y. Rychkov;
Grigori Y. Rychkov
†School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia
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Greg J. Barritt
Greg J. Barritt
1
*Department of Medical Biochemistry, School of Medicine, Flinders University, Adelaide, South Australia 5001, Australia
1To whom correspondence should be addressed (email greg.barritt@flinders.edu.au).
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Publisher: Portland Press Ltd
Received:
May 27 2008
Revision Received:
October 29 2008
Accepted:
November 13 2008
Accepted Manuscript online:
November 13 2008
Online ISSN: 1470-8728
Print ISSN: 0264-6021
© The Authors Journal compilation © 2009 Biochemical Society
2009
Biochem J (2009) 418 (3): 553–566.
Article history
Received:
May 27 2008
Revision Received:
October 29 2008
Accepted:
November 13 2008
Accepted Manuscript online:
November 13 2008
Citation
Joel Castro, Edoardo C. Aromataris, Grigori Y. Rychkov, Greg J. Barritt; A small component of the endoplasmic reticulum is required for store-operated Ca2+ channel activation in liver cells: evidence from studies using TRPV1 and taurodeoxycholic acid. Biochem J 15 March 2009; 418 (3): 553–566. doi: https://doi.org/10.1042/BJ20081052
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