Store-operated calcium entry in physiology and pathology of mammalian cells.

Targos, Berenika; Barańska, Jolanta; Pomorski, Paweł

doi:10.18388/abp.2005_3452

Cited by 51 publications

(21 citation statements)

References 102 publications

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“…It has been reported that STIM1 and Orai1 are the key components responsible for SOCE in many non-excitable cell types ( Targos et al, 2005 ; McCarl et al, 2010 ; Putney et al, 2017 ); STIM1, STIM2, and Orai1 are the main subunits of SOCs mediating SOCE in CNS neurons ( Berna-Erro et al, 2009 ; Klejman et al, 2009 ; Xia et al, 2014 ). Our RT-qPCR and Western blot results have demonstrated that the SOC family members are differentially expressed in DRGs from adult mice.…”

Section: Discussionmentioning

confidence: 99%

Orai1 and Orai3 Mediate Store-Operated Calcium Entry Contributing to Neuronal Excitability in Dorsal Root Ganglion Neurons

Wei

Mei

Xia

et al. 2017

Front. Cell. Neurosci.

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Store-operated calcium channels (SOCs) are highly calcium-selective channels that mediate calcium entry in various cell types. We have previously reported that intraplantar injection of YM-58483 (a SOC inhibitor) attenuates chronic pain. A previous study has reported that the function of SOCs in dorsal root ganglia (DRG) is enhanced after nerve injury, suggesting that SOCs may play a peripheral role in chronic pain. However, the expression, functional distribution and significance of the SOC family in DRG neurons remain elusive and the key components that mediate SOC entry (SOCE) are still controversial. Here, we demonstrated that the SOC family (STIM1, STIM2, Orai1, Orai2, and Orai3) was expressed in DRGs and STIM1 was mainly present in small- and medium-sized DRG neurons. Using confocal live cell imaging, Ca2+ imaging and electrophysiology techniques, we demonstrated that depletion of the endoplasmic reticulum Ca2+ stores induced STIM1 and STIM2 translocation, and that inhibition of STIM1 or blockage of Orai channels with pharmacological tools attenuated SOCE and SOC currents. Using the small inhibitory RNA knockdown approach, we identified STIM1, STIM2, Orai1, and Orai3 as the key components of SOCs mediating SOCE in DRG neurons. Importantly, activation of SOCs by thapsigargin induced plasma membrane depolarization and increased neuronal excitability, which were completely abolished by inhibition of SOCs or double knockdown of Orai1 and Orai3. Our findings suggest that SOCs exert an excitatory action in DRG neurons and provide a potential peripheral mechanism for modulation of pain hypersensitivity by SOC inhibition.

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Section: Discussionmentioning

confidence: 99%

Orai1 and Orai3 Mediate Store-Operated Calcium Entry Contributing to Neuronal Excitability in Dorsal Root Ganglion Neurons

Wei

Mei

Xia

et al. 2017

Front. Cell. Neurosci.

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“…[33][34][35] Foremost, TRPC1 channels in combination with ORAI1 have been implicated in CICR. [22,[34][35][36][37][38][39] TRPA1 has also been described to contribute to CICR. [40] In order to ascertain TRP channel expression in CDVs, parallel reaction monitoring (PRM) was used to specifically detect proteotypic peptides mapping to TRPC1, ORAI, TRPA1, TRPV1 or TRPV2.…”

Section: Proteome Analysismentioning

confidence: 99%

Cell-Derived Vesicles as TRPC1 Channel Delivery Systems for the Recovery of Cellular Respiratory and Proliferative Capacities

Kurth

Tai

Parate

et al. 2020

Preprint

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Pulsed electromagnetic fields (PEMFs) are capable of specifically activating a TRPC1mitochondrial axis underlying cell expansion and mitohormetic survival adaptations. This study characterizes cell-derived vesicles (CDVs) generated from C2C12 murine myoblasts and shows that they are equipped with the sufficient molecular machinery to confer mitochondrial respiratory capacity and associated proliferative responses upon their fusion with recipient cells.CDVs derived from wild type C2C12 myoblasts include the cation-permeable transient receptor potential (TRP) channels, TRPC1 and TRPA1, and directly respond to PEMF exposure with TRPC1-mediated calcium entry. By contrast, CDVs derived from C2C12 muscle cells in which TRPC1 had been genetically knocked-down using CRISPR/Cas9 genome editing, do not. Wild type C2C12-derived CDVs are also capable of restoring PEMF-induced proliferative and mitochondrial activation in two C2C12-derived TRPC1 knockdown clonal cell lines in accordance to their endogenous degree of TRPC1 suppression. C2C12 wild type CDVs respond to menthol with calcium entry and accumulation, likewise verifying TRPA1 functional gating and further corroborating compartmental integrity. Proteomic and lipidomic analyses confirm the surface membrane origin of the CDVs providing an initial indication of the minimal cellular machinery required to recover mitochondrial function. CDVs hence possess the potential of restoring respiratory and proliferative capacities to senescent cells and tissues.

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“…) and has been shown to be involved in conditions such as neuropathic pain, ischaemic stroke, Parkinson's disease and Alzheimer's disease (Targos et al . ; Berna‐Erro et al . ; Selvaraj et al .…”

Section: Introductionmentioning

confidence: 99%

Native store‐operated calcium channels are functionally expressed in mouse spinal cord dorsal horn neurons and regulate resting calcium homeostasis

Xia

Rong

Gao

et al. 2014

The Journal of Physiology

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Key pointsr A previous study indicates that store-operated calcium channels (SOCs) play a role in pain hypersensitivity. Here we report for the first time that SOCs are expressed and functional in spinal cord dorsal horn neurons. r The present study reveals that a novel calcium signal mediated by SOCs is present in dorsal horn neurons and provides a potential mechanism for SOC inhibition-induced central analgesia.Abstract Store-operated calcium channels (SOCs) are calcium-selective cation channels that mediate calcium entry in many different cell types. Store-operated calcium entry (SOCE) is involved in various cellular functions. Increasing evidence suggests that impairment of SOCE is responsible for numerous disorders. A previous study demonstrated that YM-58483, a potent SOC inhibitor, strongly attenuates chronic pain by systemic or intrathecal injection and completely blocks the second phase of formalin-induced spontaneous nocifensive behaviour, suggesting a potential role of SOCs in central sensitization. However, the expression of SOCs, their molecular identity and function in spinal cord dorsal horn neurons remain elusive. Here, we demonstrate that SOCs are expressed in dorsal horn neurons. Depletion of calcium stores from the endoplasmic reticulum (ER) induced large sustained calcium entry, which was blocked by SOC inhibitors, but not by voltage-gated calcium channel blockers. Depletion of ER calcium stores activated inward calcium-selective currents, which was reduced by replacing Ca 2+ with Ba 2+ and reversed by SOC inhibitors. Using the small inhibitory RNA knockdown approach, we identified both STIM1 and STIM2 as important mediators of SOCE and SOC current, and Orai1 as a key component of the Ca 2+ release-activated Ca 2+ channels in dorsal horn neurons. Knockdown of STIM1, STIM2 or Orai1 decreased resting Ca 2+ levels. We also found that activation of neurokinin 1 receptors led to SOCE and activation of SOCs produced an excitatory action in dorsal horn neurons. Our findings reveal that a novel SOC signal is present in dorsal horn neurons and may play an important role in pain transmission.

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Store-operated calcium entry in physiology and pathology of mammalian cells.

Cited by 51 publications

References 102 publications

Orai1 and Orai3 Mediate Store-Operated Calcium Entry Contributing to Neuronal Excitability in Dorsal Root Ganglion Neurons

Orai1 and Orai3 Mediate Store-Operated Calcium Entry Contributing to Neuronal Excitability in Dorsal Root Ganglion Neurons

Cell-Derived Vesicles as TRPC1 Channel Delivery Systems for the Recovery of Cellular Respiratory and Proliferative Capacities

Native store‐operated calcium channels are functionally expressed in mouse spinal cord dorsal horn neurons and regulate resting calcium homeostasis

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