Focal agonist stimulation results in spatially restricted Ca<sup>2+</sup> release and capacitative Ca<sup>2+</sup> entry in bovine vascular endothelial cells

Hüser, Jörg; Holda, Jaclyn R.; Kockskämper, Jens; Blatter, Lothar A.

doi:10.1111/j.1469-7793.1999.101af.x

Cited by 24 publications

(20 citation statements)

References 28 publications

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“…On the other hand, ATP induces Ca 2+ i responses both in early and organized tubules in vitro. In contrast to AA, ATP binding to its specific G-protein -coupled P2Y receptors triggers a strong and fast Ca 2+ release from intracellular stores via IP3 production, followed by a sustained store-operated Ca 2+ entry (47). The lack of a tubulogenic effect and the unaltered ATP-induced Ca 2+ i signals during the capillary-like network development support the hypothesis of a specific role for AAinduced Ca 2+ i signals in the early steps of B-TEC in vitro angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Fiorio

Grange

Antoniotti

et al. 2008

Molecular Cancer Research

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Growth factor -induced intracellular calcium signals in endothelial cells regulate cytosolic and nuclear events involved in the angiogenic process. Among the intracellular messengers released after proangiogenic stimulation, arachidonic acid (AA) plays a key role and its effects are strictly related to calcium homeostasis and cell proliferation. Here, we studied AA-induced intracellular calcium signals in endothelial cells derived from human breast carcinomas (B-TEC). AA promotes B-TEC proliferation and organization of vessel-like structures in vitro. The effect is directly mediated by the fatty acid without a significant contribution of its metabolites. AA induces Ca 2+ i signals in the entire capillary-like structure during the early phases of tubulogenesis in vitro. No such responses are detectable in B-TECs organized in more structured tubules. In B-TECs growing in monolayer, AA induces two different signals: a Ca 2+ i increase due to Ca 2+ entry and an inhibition of store-dependent Ca 2+ entry induced by thapsigargin or ATP. An inhibitor of Ca 2+ entry and angiogenesis, carboxyamidotriazole, significantly and specifically decreases AA-induced B-TEC tubulogenesis, as well as AA-induced Ca 2+ signals in B-TECs. We conclude that (a) AA-activated Ca 2+ entry is associated with the progression through the early phases of angiogenesis, mainly involving proliferation and tubulogenesis, and it is down-regulated during the reorganization of tumor-derived endothelial cells in capillary-like structures; and (b) inhibition of AA-induced Ca 2+ entry may contribute to the antiangiogenic action of carboxyamidotriazole. (Mol Cancer Res 2008;6(4):535 -45)

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Section: Discussionmentioning

confidence: 99%

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Fiorio

Grange

Antoniotti

et al. 2008

Molecular Cancer Research

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“…The ability of intracellular BAPTA to slow reloading, and of Ba 2+ and Mn 2+ , which are not transported by Ca 2+ pumps, to enter the cytosolic pool following store depletion, was taken as evidence that Ca 2+ entering the cell traverses a narrow gap of cytosol before being actively pumped into the ER [17]. Later studies of Xenopus oocytes, endothelial cells and astrocytes showed that local receptor stimulation evoked Ca 2+ entry (as detected by Cl − channel activation or Ca 2+ -dependent dye signals) that was confined to within 10's to 100's of μm from where Ca 2+ release was thought to occur [18][19][20][21].…”

Section: Communication Between Ca 2+ Stores and The Crac Channel: Locmentioning

confidence: 99%

“…The only available marker for active CRAC channels is the elevated [Ca 2+ ] i microdomains that form near open channels. Several prior studies using Ca 2+ -sensitive dyes have shown that SOCE occurs within 10-100 μM of the ER [19][20][21], but the applied imaging techniques lacked sufficient resolution to pinpoint the relationship between individual influx sites and junctional ER structures. Much higher resolution is possible with TIRF microscopy, which has been used to image Ca 2+ microdomains near voltage-gated Ca 2+ (Ca V ) channels on a submicron scale [67,68].…”

Section: The Dynamic Dyad: Defining the Elementary Unit Of Store-opermentioning

confidence: 99%

Some assembly required: Constructing the elementary units of store-operated Ca2+ entry

Luik

Lewis

2007

Cell Calcium

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SUMMARYThe means by which Ca 2+ store depletion evokes the opening of store-operated Ca 2+ channels (SOCs) in the plasma membrane of excitable and non-excitable cells has been a longstanding mystery. Indirect evidence has supported local interactions between the ER and SOCs as well as long-range interactions mediated through a diffusible activator. The recent molecular identification of the ER Ca 2+ sensor (STIM1) and a subunit of the CRAC channel (Orai1), a prototypic SOC, has now made it possible to visualize directly the sequence of events that links store depletion to CRAC channel opening. Following store depletion, STIM1 moves from locations throughout the ER to accumulate in ER subregions positioned within 10-25 nm of the plasma membrane. Simultaneously, Orai1 gathers at discrete sites in the plasma membrane directly opposite STIM1, resulting in local CRAC channel activation. These new studies define the elementary units of store-operated Ca 2+ entry, and reveal an unprecedented mechanism for channel activation in which the stimulus brings a channel and its activator/sensor together for interaction across apposed membrane compartments. We discuss the implications of this choreographic mechanism with regard to Ca 2+ dynamics, specificity of Ca 2+ signaling, and the existence of a specialized ER subset dedicated to the control of the CRAC channel.

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“…In calf pulmonary artery endothelial cells (CPAEs), elementary events precede the onset of the massive ATPinduced Ca 2+ release from intracellular stores, leading to the vasoactive response [5,6].…”

Section: Introductionmentioning

confidence: 99%

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

Munaron

2009

TOBIOJ

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Angiogenic factors, including bFGF and VEGF, induce cytosolic calcium (Ca c ) increases in endothelial cells, critically involved in angiogenesis progression. At low agonist concentrations, Ca c elevation is mainly due to calcium entry controlled by a complex interplay between two intracellular messengers, arachidonic acid (AA) and nitric oxide (NO), released upon stimulation with proangiogenic factors: they trigger spatially localized calcium signals restricted to the cell periphery, and such a spatiotemporal pattern could contribute to the specificity of cellular responses.Based on experimental measurements, here we provide the first quantitative spatiotemporal 3D modeling of proangiogenic calcium events in endothelial cells using Virtual Cell framework. The main aims were to validate previously proposed signaling pathways and to suggest new experimental protocols.The most relevant conclusions are: 1. The interplay between AA and NO, previously proposed to be responsible for VEGF/bFGF-dependent calcium entry in endothelial cells, triggers peripheral calcium signals that reproduce the experimental measurements; 2. Spatial restriction is not an artefact due to the calcium-sensitive dye; 3. Channels clusterization in thin lamellipodia plays a key role in the generation of the peripheral-restricted proangiogenic calcium signals; 4. A model containing two distinct channels, named AAAC and NOAC, respectively activated by AA or NO, explains the basic properties of proangiogenic calcium signals.This could be considered an 'open model' containing the simplest conditions leading to a satisfactory reproduction of the experimental results: it should be implemented in order to make it more complete and to maximize physical and biochemical constraints.

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Focal agonist stimulation results in spatially restricted Ca²⁺ release and capacitative Ca²⁺ entry in bovine vascular endothelial cells

Cited by 24 publications

References 28 publications

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Some assembly required: Constructing the elementary units of store-operated Ca2+ entry

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

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Focal agonist stimulation results in spatially restricted Ca2+ release and capacitative Ca2+ entry in bovine vascular endothelial cells

Cited by 24 publications

References 28 publications

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Some assembly required: Constructing the elementary units of store-operated Ca2+ entry

A Tridimensional Model of Proangiogenic Calcium Signals in Endothelial Cells

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Focal agonist stimulation results in spatially restricted Ca²⁺ release and capacitative Ca²⁺ entry in bovine vascular endothelial cells