STIM1/Orai1-mediated store-operated Ca2+ entry: the tip of the iceberg

Giachini, Fernanda R.; Lima, Victor Vitorino; Hannan, Johanna L.; Carneiro, Fernando S.; Webb, R.; Tostes, Rita C.

doi:10.1590/s0100-879x2011007500133

Cited by 12 publications

(12 citation statements)

References 57 publications

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“…These Stim1 oligomers migrate towards sites of the ER that are in close vicinity to the plasma membrane, where they assembly into punctuate clusters and activate SOCE by directly binding to Orai1 [335,336] . Accordingly, the latter has been found to be an essential component of SOCE by forming the pore unit of the channel in a variety of cell types [335,337] , including vascular ECs [205,206,338] . Orai1 is a four-transmembrane protein with intracellular NH2 and COOH termini.…”

Section: Stim1 and Orai1mentioning

confidence: 99%

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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Section: Stim1 and Orai1mentioning

confidence: 99%

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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“…Exaggerated vascular smooth muscle cell (VSMC) proliferative responses have been widely described as underlying mechanisms of aberrant neointima formation in vascular diseases (Giachini et al, ; Miao, Murakami, Song, Chao, & Chao, ). A hallmark of vascular pathologies is the presence of elevated levels of vasoactive peptides, such as angiotensin‐II (Ang‐II), which is a major vasoconstrictor with a demonstrated causal role in the pathophysiology of vascular disorders (Montezano, Nguyen Dinh, Rios, & Touyz, ).…”

Section: Introductionmentioning

confidence: 99%

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

Simo‐Cheyou

Tan

Grygorczyk

et al. 2017

Journal Cellular Physiology

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An upregulation of Egr-1 expression has been reported in models of atherosclerosis and intimal hyperplasia and, various vasoactive peptides and growth promoting stimuli have been shown to induce the expression of Egr-1 in vascular smooth muscle cells (VSMC). Angiotensin-II (Ang-II) is a key vasoactive peptide that has been implicated in the pathogenesis of vascular diseases. Ang-II elevates intracellular Ca through activation of the store-operated calcium entry (SOCE) involving an inositol-3-phosphate receptor (IP3R)-coupled depletion of endoplasmic reticular Ca and a subsequent activation of the stromal interaction molecule 1 (STIM-1)/Orai-1 complex. However, the involvement of IP3R/STIM-1/Orai-1-Ca -dependent signaling in Egr-1 expression in VSMC remains unexplored. Therefore, in the present studies, we have examined the role of Ca signaling in Ang-II-induced Egr-1 expression in VSMC and investigated the contribution of STIM-1 or Orai-1 in mediating this response. 2-aminoethoxydiphenyl borate (2-APB), a dual non-competitive antagonist of IP3R and inhibitor of SOCE, decreased Ang-II-induced Ca release and attenuated Ang-II-induced enhanced expression of Egr-1 protein and mRNA levels. Egr-1 upregulation was also suppressed following blockade of calmodulin and CaMKII. Furthermore, RNA interference-mediated depletion of STIM-1 or Orai-1 attenuated Ang-II-induced Egr-1 expression as well as Ang-II-induced phosphorylation of ERK1/2 and CREB. In addition, siRNA-induced silencing of CREB resulted in a reduction in the expression of Egr-1 stimulated by Ang-II. In summary, our data demonstrate that Ang-II-induced Egr-1 expression is mediated by STIM-1/Orai-1/Ca -dependent signaling pathways in A-10 VSMC.

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“…70 An interesting observation is that Orai1 expression appears higher in males compared with females, and the suggestion that higher Orai1 levels in males might explain the known propensity of males to develop cardiovascular diseases compared with females and the well-documented protective cardiovascular effects of female sex hormones in pre-menopausal women. 71,72 Whether an increased expression of Orai3 relative to Orai1 in the cardiovascular system is a characteristic of females is unknown. If this is indeed the case, the functional outcome of Orai3 upregulation in the cardiovascular system is an important question that warrants further investigations.…”

Section: Orai3 In Breast Cancermentioning

confidence: 99%

Emerging roles of Orai3 in pathophysiology

et al. 2013

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STIM1/Orai1-mediated store-operated Ca2+ entry: the tip of the iceberg

Cited by 12 publications

References 57 publications

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

Emerging roles of Orai3 in pathophysiology

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STIM1/Orai1-mediated store-operated Ca2+ entry: the tip of the iceberg

Cited by 12 publications

References 57 publications

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

Emerging roles of Orai3 in pathophysiology

Contact Info

Product

Resources

About

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters