Journal
BIOCHEMICAL JOURNAL
Volume 418, Issue -, Pages 553-566Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20081052
Keywords
bile acids; calcium release; endoplasmic reticulum; stromal interaction molecule 1 (STIM1); store-operated calcium entry; transient receptor potential vanilloid 1 (TRPV1)
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Funding
- Australian Research Council [DP0559562]
- Flinders Medical Centre Foundation, South Australia
- Australian Research Council [DP0559562] Funding Source: Australian Research Council
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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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