Cloning and Functional Expression of a Human Ca2+-Permeable Cation Channel Activated by Calcium Store Depletion

Zitt, Christof; Zobel, Andrea; Obukhov, Alexander G.; Harteneck, Christian; Kalkbrenner, Frank; Lückhoff, Andreas; Schultz, Günter

doi:10.1016/s0896-6273(00)80145-2

Cited by 369 publications

(293 citation statements)

References 25 publications

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“…This subfamily includes seven members (TRPC1-TRPC7) that exhibit various properties, regulation mechanisms, and physiological functions. Interestingly, in 1996, almost a decade before STIM1 was discovered, TRPC1 had been identified as a potential SOC candidate (154), and this was subsequently confirmed in many cell types including both nonexcitable and excitable cells (84,138,139). Although the role of other TRPCs (TRPC2-7) in SOCE remains poorly understood, over the last decade TRPC3 (79), TRPC4 (71), and TRPC6 (79) have all been implicated in SOCE-mediated hypertrophic signaling in cardiomyocytes.…”

Section: Orai1/trpcmentioning

confidence: 99%

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

Collins

Zhu-Mauldin

Marchase

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

111

102

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Collins HE, Zhu-Mauldin X, Marchase RB, Chatham JC. STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology. Am J Physiol Heart Circ Physiol 305: H446 -H458, 2013. First published June 21, 2013 doi:10.1152/ajpheart.00104.2013.-Store-operated Ca 2ϩ entry (SOCE) is critical for Ca 2ϩ signaling in nonexcitable cells; however, its role in the regulation of cardiomyocyte Ca 2ϩ homeostasis has only recently been investigated. The increased understanding of the role of stromal interaction molecule 1 (STIM1) in regulating SOCE combined with recent studies demonstrating the presence of STIM1 in cardiomyocytes provides support that this pathway co-exists in the heart with the more widely recognized Ca 2ϩ handling pathways associated with excitation-contraction coupling. There is now substantial evidence that STIM1-mediated SOCE plays a key role in mediating cardiomyocyte hypertrophy, both in vitro and in vivo, and there is growing support for the contribution of SOCE to Ca 2ϩ overload associated with ischemia/reperfusion injury. Here, we provide an overview of our current understanding of the molecular regulation of SOCE and discuss the evidence supporting the role of STIM1/Orai1-mediated SOCE in regulating cardiomyocyte function.store-operated Ca 2ϩ entry; stromal interaction molecule 1; orai1; cardiomyocytes STORE-OPERATED CA 2ϩ ENTRY (SOCE), also known as capacitative calcium entry (CCE), is the major mechanism of Ca 2ϩ entry in nearly all nonexcitable cells (97, 99). In addition, it is increasingly recognized to co-exist with voltage-gated Ca 2ϩ channels in excitable cells, including neurons, skeletal muscle cells, and cardiomyocytes (1,38,45,83,121). In response to inositol 1,4,5-triphosphate (IP 3 )-(43) or ryanodine receptor (RyR)-mediated (3) Ca 2ϩ release from ER/SR stores, SOCE facilitates the influx of Ca 2ϩ from the extracellular space, resulting in a sustained increase in cytosolic Ca 2ϩ levels. Thus, although one of the roles of SOCE is to rapidly refill the depleted ER/SR stores, the subsequent sustained increase in cytosolic Ca 2ϩ also regulates numerous gene transcription pathways (33,50,151). Indeed, aberrant SOCE has been observed in a growing number of diseases including severe combined immunodeficiency, acute pancreatitis, and Alzheimer's disease (86).The integration of SOCE into well-established models of Ca 2ϩ homeostasis was hampered for many years by the lack of specific molecular mediators; even as recently as 2004 there was considerable controversy as to the specific mechanisms regulating SOCE (90, 113). However, in 2005, stromal interaction molecule 1 (STIM1) was found to localize to the ER/SR membrane and shown to function as a primary mediator of SOCE (54, 102). The putative physiological and pathophysiological roles of SOCE and STIM1 that have been identified to date are summarized in Table 1. A number of studies have recently reported the presence of STIM1 in adult cardiomyocytes (37,59,153), and consistent with earlier evidence supporting a rol...

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Section: Orai1/trpcmentioning

confidence: 99%

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

Collins

Zhu-Mauldin

Marchase

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

111

102

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“…however, we initially asked whether cholesterol might regulate raft trafficking of TRPC1. TRPC1 is a prototypical TRPC protein that can both localize to rafts and transmit nonspecific Ca 2ϩ entry currents (9,20,(41)(42)(43)(44).…”

Section: Cholesterol Causes Trpc1 Trafficking To Lipid Raftsmentioning

confidence: 99%

Free Cholesterol Alters Lipid Raft Structure and Function Regulating Neutrophil Ca2+ Entry and Respiratory Burst: Correlations with Calcium Channel Raft Trafficking

Kannan

Barlos

Hauser

2007

The Journal of Immunology

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Recent studies associate cholesterol excess and atherosclerosis with inflammation. The link between these processes is not understood, but cholesterol is an important component of lipid rafts. Rafts are thought to concentrate membrane signaling molecules and thus regulate cell signaling through G protein-coupled pathways. We used methyl β-cyclodextrin to deplete cholesterol from polymorphonuclear neutrophil (PMN) rafts and thus study the effects of raft disruption on G protein-coupled Ca2+ mobilization. Methyl β-cyclodextrin had no effect on Ca2+ store depletion by the G protein-coupled agonists platelet-activating factor or fMLP, but abolished agonist-stimulated Ca2+ entry. Free cholesterol at very low concentrations regulated Ca2+ entry into PMN via nonspecific Ca2+ channels in a biphasic fashion. The specificity of cholesterol regulation for Ca2+ entry was confirmed using thapsigargin studies. Responses to cholesterol appear physiologic because they regulate respiratory burst in a proportional biphasic fashion. Investigating further, we found that free cholesterol accumulated in PMN lipid raft fractions, promoting formation and polarization of membrane rafts. Finally, the transient receptor potential calcium channel protein TRPC1 redistributed to raft fractions in response to cholesterol. The uniformly biphasic relationships between cholesterol availability, Ca2+ signaling and respiratory burst suggest that Ca2+ influx and PMN activation are regulated by the quantitative relationships between cholesterol and other environmental lipid raft components. The association between symptomatic cholesterol excess and inflammation may therefore in part reflect free cholesterol- dependent changes in lipid raft structure that regulate immune cell Ca2+ entry. Ca2+ entry-dependent responses in other cell types may also reflect cholesterol bioavailability and lipid incorporation into rafts.

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“…[21][22][23] This superfamily of proteins is comprised of three branches distinguished by sequence homology and functional similarities: TRPC (canonical), TRPV (vanilloid) and TRPM (melastatin). 24 Two subgroups within the canonical branch, (TRPC1,4&5 and TRPC3,6&7, respectively) have been implicated in SOCE and ROCE, 24,25 raising the prospect of the involvement of one or more of these TRPC members in the Ca 2 þ abnormalities that have been reported in BD and the in actions of Li in BLCLs highlighted above.…”

Section: Introductionmentioning

confidence: 99%

Chronic lithium treatment of B lymphoblasts from bipolar disorder patients reduces transient receptor potential channel 3 levels

et al. 2004

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Chronic lithium treatment of B-lymphoblast cell lines (BLCLs) from bipolar-I disorder (BD-I) patients and healthy subjects ex vivo attenuates agonist-and thapsigargin-stimulated intracellular calcium (Ca 2 þ ) responses. As these findings suggest that chronic lithium treatment modifies receptor (ROCE) and/or store-operated Ca 2 þ entry (SOCE) mechanisms, we determined whether chronic lithium treatment of BLCLs modified the expression of two members of the transient receptor potential channels (TRPC1 & 3), which participate in ROCE/SOCE. Chronic lithium treatment significantly reduced BLCL TRPC3 immunoreactivity (repeated-measures ANOVA, P ¼ 0.00005), with interaction effects of diagnosis (P ¼ 0.037) and sex (P ¼ 0.040). The lithium-induced decrease was greatest in BLCLs from female BD-I patients compared with those from healthy females (À27%) and with vehicle-treated BLCLs from female BD-I patients (À33%). However, lithium treatment did not affect TRPC1 and 3 mRNA levels, and TRPC1 immunoreactivity. Downregulation of TRPC3 may be an important mechanism by which lithium ameliorates pathophysiological Ca 2 þ disturbances as observed in BD.

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Cloning and Functional Expression of a Human Ca2+-Permeable Cation Channel Activated by Calcium Store Depletion

Cited by 369 publications

References 25 publications

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology

Free Cholesterol Alters Lipid Raft Structure and Function Regulating Neutrophil Ca2+ Entry and Respiratory Burst: Correlations with Calcium Channel Raft Trafficking

Chronic lithium treatment of B lymphoblasts from bipolar disorder patients reduces transient receptor potential channel 3 levels

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