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, Edoardo C. Aromataris, Grigori Y. Rychkov, Greg J. Barritt

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

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 agonistsensitive 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 fromwhich 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.

LanguageEnglish
Pages553-566
Number of pages14
JournalBiochemical Journal
Volume418
Issue number3
DOIs
Publication statusPublished - 15 Mar 2009

Keywords

  • Bile acids
  • Calcium release
  • Endoplasmic reticulum
  • Store-operated calcium entry
  • Stromal interaction molecule 1 (STIM1)
  • Transient receptor potential vanilloid 1 (TRPV1)

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

@article{2608948cb7694619a749bf4a69c33c72,
title = "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",
abstract = "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 agonistsensitive 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 fromwhich 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.",
keywords = "Bile acids, Calcium release, Endoplasmic reticulum, Store-operated calcium entry, Stromal interaction molecule 1 (STIM1), Transient receptor potential vanilloid 1 (TRPV1)",
author = "Joel Castro and Aromataris, {Edoardo C.} and Rychkov, {Grigori Y.} and Barritt, {Greg J.}",
year = "2009",
month = "3",
day = "15",
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language = "English",
volume = "418",
pages = "553--566",
journal = "Biochemical Journal",
issn = "0264-6021",
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T1 - A small component of the endoplasmic reticulum is required for store-operated Ca2+ channel activation in liver cells

T2 - Biochemical Journal

AU - Castro, Joel

AU - Aromataris, Edoardo C.

AU - Rychkov, Grigori Y.

AU - Barritt, Greg J.

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Y1 - 2009/3/15

N2 - 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 agonistsensitive 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 fromwhich 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.

AB - 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 agonistsensitive 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 fromwhich 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.

KW - Bile acids

KW - Calcium release

KW - Endoplasmic reticulum

KW - Store-operated calcium entry

KW - Stromal interaction molecule 1 (STIM1)

KW - Transient receptor potential vanilloid 1 (TRPV1)

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U2 - 10.1042/BJ20081052

DO - 10.1042/BJ20081052

M3 - Article

VL - 418

SP - 553

EP - 566

JO - Biochemical Journal

JF - Biochemical Journal

SN - 0264-6021

IS - 3

ER -