Subpopulation of Store-operated Ca2+ Channels Regulate Ca2+-induced Ca2+ Release in Non-excitable Cells

Yao, Jian; Li, Qin; Chen, Jin; Muallem, Shmuel

doi:10.1074/jbc.m314028200

Cited by 16 publications

(19 citation statements)

References 44 publications

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“…These data are inconsistent with the Fura-2 data, which demonstrate that 1 M and 1 nM Tg activate similar magnitude of SOCE, although activation is slower at the lower [Tg]. We hypothesized that this discrepancy could be due to a contribution of Ca 2ϩ -induced Ca 2ϩ release to the Fura-2 fluorescence measurements (28). Alternatively, it could be a result of recycling of Ca 2ϩ into the ER store by residual SERCA activity in cells treated with the lower [Tg].…”

Section: Methodscontrasting

confidence: 56%

Relocalization of STIM1 for Activation of Store-operated Ca2+ Entry Is Determined by the Depletion of Subplasma Membrane Endoplasmic Reticulum Ca2+ Store

Ong

Liu

Tsaneva-Atanasova

et al. 2007

Journal of Biological Chemistry

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entering the cell is rapidly taken up into the ER by SERCA activity with minimal diffusion in the subplasma membrane region. These studies indicate close apposition of the ER and plasma membrane at the site of SOCE (1-6). Thus, it has been suggested that ER localized in the subplasma membrane region is likely to be coupled to SOCE and that depletion of these local Ca 2ϩ stores triggers activation of SOCE. The presently proposed mechanisms for activation of SOCE suggest direct physical coupling between components in the ER and plasma membrane, generation of diffusible components, or recruitment of the SOC channel. The exact mechanism involved in regulation of SOCE as well as the molecular components of the channel(s) mediating Ca 2ϩ entry in different types of cells has not been clearly identified.Recent studies have suggested STIM1 (stromal interacting molecule 1) as a novel regulator for SOCE. STIM1, which is a Ca 2ϩ -binding protein localized diffusely in the ER, has been shown to relocate into a peripheral region of the cell in response to internal Ca 2ϩ store depletion (7,8). STIM1 displays punctate subplasma membrane localization in response to depletion of intracellular Ca 2ϩ stores, which has been reported to be causal in activation of SOCE and to define the elementary unit that is involved in SOCE. Although several studies have clearly established involvement of ER-plasma membrane junctional domains in the regulation of SOCE, the exact site of store depletion has not yet been demonstrated. Based on all of the data available presently, it is logical to propose that that since the EF-hand domain of STIM1 is localized in the lumen of the ER and STIM1 punctae involved in SOCE activation are localized in subplasma membrane Ca 2ϩ stores very close to the surface * The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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Section: Methodscontrasting

confidence: 56%

Relocalization of STIM1 for Activation of Store-operated Ca2+ Entry Is Determined by the Depletion of Subplasma Membrane Endoplasmic Reticulum Ca2+ Store

Ong

Liu

Tsaneva-Atanasova

et al. 2007

Journal of Biological Chemistry

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“…5). In an earlier work (Yao et al, 2004) we showed that treatment with 10 M CPA for 2 minutes releases only a small fraction of the intracellular Ca 2+ pool, but is sufficient to activate Ca 2+ influx that triggers the CICR mechanism. The first CICR event in response to 7.5 mM Ca (403±37 and 312±35, n=5).…”

Section: Resultsmentioning

confidence: 99%

“…The ER module of the Ca 2+ -signaling complex includes the IP 3 receptors and the sarco/endoplasmic reticulum Ca 2+ pump (SERCA) (Berridge et al, 2000;Kiselyov et al, 2003). In specialized cells, such as salivary gland cells (Lee et al, 1997;Yao et al, 2004) and urinary bladder smooth muscle (UBSM) cells (Wegener et al, 2004) (Wegener et al, 2004). Depletion of ER Ca 2+ triggers ER stress and activates PERK (Harding et al, 1999), which is also observed in cells responding to physiological secretory agonists (Alcazar et al, 1997;Kimball and Jefferson, 1990;Kimball and Jefferson, 1991 (Berridge et al, 2000;Kiselyov et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

ER stress disrupts Ca2+-signaling complexes and Ca2+ regulation in secretory and muscle cells from PERK-knockout mice

Huang

Yao

Zeng

et al. 2006

Journal of Cell Science

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“…We call these store-operated Ca 2+ channels (SOCCs) or capacitative Ca 2+ entry (CCE) channels. Previous studies have suggested SOCCs are restricted in non-excitable cells [8,9] , but they have only recently been investigated in excitable cells , such as smooth muscle cells and neurons, which are involved in smooth muscle tone and regulation of synaptic plasticity. It has been reported there is a relationship between CCE and the regulation of smooth muscle tone with respect to their involvement in pulmonary, stomach, bronchial, vascular, gallbladder, and basilar artery tissue [10][11][12][13][14][15] .…”

Section: Camentioning

confidence: 99%

Sources of calcium in agonist-induced contraction of rat distal colon smooth muscle in vitro

Zhou

De-hu²,

Pan³

et al. 2008

WJG

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AIM:To study the origin of calcium necessary for agonist-induced contraction of the distal colon in rats. METHODS:The change in intracel lular calcium concentration ([Ca 2+ ]i) evoked by elevating external Ca 2+ was detected by fura 2/AM fluorescence. Contractile activity was measured with a force displacement transducer. Tension was continuously monitored and recorded using a Powerlab 4/25T data acquisition system with an ML110 bridge bioelectric physiographic amplifier. RESULTS:Store depletion induced Ca 2+ influx had an effect on [Ca 2+ ]i. In nominally Ca 2+ -free medium, the sarco-endoplasmic reticulum Ca 2+ -ATPase inhibitor thapsigargin (1 µmol/L) increased [Ca 2+ ]i from 68 to 241 nmol/L, and to 458 (P < 0.01) and 1006 nmol/L (P < 0.01), respectively, when 1.5 mmol/L and 3.0 mmol/L extracellular Ca 2+ was reintroduced. Furthermore, the change in [Ca 2+ ]i was observed with verapamil (5 µmol/L), La 3+ (1 mmol/L) or KCl (40 mmol/L) in the bathing solution. These channels were sensitive to La 3+ (P < 0.01), insensitive to verapamil, and voltage independent. In isolated distal colons we found that in normal Krebs solution, contraction induced by acetylcholine (ACh) was partially inhibited by verapamil, and the inhibitory rate was 41% (P < 0.05). On the other hand, in Ca 2+ -free Krebs solution, ACh induced transient contraction due to Ca 2+ release from the intracellular stores. The transient contraction lasted until the Ca 2+ store was depleted. Restoration of extracellular Ca 2+ in the presence of atropine produced contraction, mainly due to Ca 2+ influx. Such contraction was not inhibited by verapamil, but was decreased by La 3+ (50 µmol/L) from 0.96 to 0.72 g (P < 0.01). CONCLUSION:The predominant source of activator C a 2 + f o r t h e c o n t ra c t i l e r e s p o n s e t o a g o n i s t i s extracellular Ca 2+ , and intracellular Ca 2+ has little role to play in mediating excitation-contraction coupling by agonists in rat distal colon smooth muscle in vitro . The influx of extracellular Ca 2+ is mainly mediated through voltage-, receptor-and store-operated Ca 2+ channels, which can be used as an alternative to develop new drugs targeted on the dysfunction of digestive tract motility.

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Subpopulation of Store-operated Ca2+ Channels Regulate Ca2+-induced Ca2+ Release in Non-excitable Cells

Abstract: Ca2؉ -induced Ca 2؉ release (CICR) is a well characterized activity in skeletal and cardiac muscles mediated by the ryanodine receptors. The present study demonstrates CICR in the non-excitable parotid acinar cells, which resembles the mechanism described in cardiac myocytes.

Cited by 16 publications

References 44 publications

Relocalization of STIM1 for Activation of Store-operated Ca2+ Entry Is Determined by the Depletion of Subplasma Membrane Endoplasmic Reticulum Ca2+ Store

Relocalization of STIM1 for Activation of Store-operated Ca2+ Entry Is Determined by the Depletion of Subplasma Membrane Endoplasmic Reticulum Ca2+ Store

ER stress disrupts Ca2+-signaling complexes and Ca2+ regulation in secretory and muscle cells from PERK-knockout mice

Sources of calcium in agonist-induced contraction of rat distal colon smooth muscle in vitro

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