Ca2+-dependent synthesis of prostaglandin I2 and mobilization of arachidonic acid from phospholipids in cultured endothelial cells permeabilized with saponin

Martin, Thomas W.; Michaelis, Kevin C.

doi:10.1016/0167-4889(90)90237-8

Cited by 12 publications

(11 citation statements)

References 56 publications

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“…In PASMCs, changes in [Ca 2+ ] i modulate contraction(Buckley et al, 1995; Busse and Mulsch, 1990; Emori et al, 1989; Kohno et al, 1992; Martin and Michaelis, 1990; Whorton et al, 1984), cell proliferation and growth by facilitating progression through the cell cycle(Mogami and Kojima, 1993; Rodman et al, 2005; Shukla et al, 2005) and the activation of genes via regulation of Ca 2+ -sensitive transcription factors(Altura et al, 2003; Ginty et al, 1991; Hardingham et al, 1998; Pribnow et al, 1992; Rothman et al, 1994). That Ca 2+ signaling plays a crucial role in a wide array of cell functions underscores the importance of understanding the mechanisms regulating Ca 2+ homeostasis under both physiologic and pathophysiologic conditions.…”

Section: Ca2+ Signaling In Pasmcsmentioning

confidence: 99%

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Shimoda

Undem

2010

Respiratory Physiology & Neurobiology

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In contrast to the systemic vasculature, where hypoxia causes vasodilation, pulmonary arteries constrict in response to hypoxia. The mechanisms underlying this unique response have been the subject of investigation for over 50 years, and still remain a topic of great debate. Over the last 20 years, there has emerged a general consensus that both increases in intracellular calcium concentration and changes in reactive oxygen species (ROS) generation play key roles in the pulmonary vascular response to hypoxia. Controversy exists, however, regarding whether ROS increase or decrease during hypoxia, the source of ROS, and the mechanisms by which changes in ROS might impact intracellular calcium, and vice versa. This review will discuss the mechanisms regulating [Ca 2+ ] i and ROS in PASMCs, and the interaction between ROS and Ca 2+ signaling during exposure to acute hypoxia.

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Section: Ca2+ Signaling In Pasmcsmentioning

confidence: 99%

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Shimoda

Undem

2010

Respiratory Physiology & Neurobiology

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“…The production of vasodilator factors such as nitric oxide ( via constituitive NO synthase) and prostacyclin ( via cyclo‐oxygenase) by endothelial cells represent Ca 2+ ‐dependent processes (for example see references Martin & Michaelis, 1990; Lin et al ., 2000; Mizuno et al ., 2000). The increase in intracellular Ca 2+ typically occurs following the activation of membrane receptors which initiate signal transduction pathways that lead to Ca 2+ release from the endoplasmic reticulum (ER) and entry from the extracellular compartment.…”

Section: Introductionmentioning

confidence: 99%

Capacitative Ca²⁺ entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C

Bishara

Murphy

Hill

2002

British J Pharmacology

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1 Agonists increase endothelial cell intracellular Ca 2+ , in part, by capacitative entry, which is triggered by the ®lling state of intracellular Ca 2+ stores. It has been suggested that depletion of endoplasmic reticulum (ER) Ca 2+ stores either leads to a physical coupling between the ER and a plasma membrane channel, or results in production of an intracellular messenger which a ects the gating of membrane channels. As an axis involving the IP 3 receptor has been implicated in a physical coupling mechanism the aim of this study was to examine the e ects of the putative IP 3 receptor antagonists/modulators, 2 aminoethoxydiphenyl borate (2APB) and xestospongin C, on endothelial cell Ca 2+ entry. 2 Studies were conducted in fura 2 loaded cultured bovine aortic endothelial cells and endothelial cells isolated from rat heart. 3 2APB (30 ± 300 mM) inhibited Ca 2+ entry induced by both agonists (ATP 1 mM, bradykinin 0.1 mM) and receptor-independent mechanisms (thapsigargin 1 mM, ionomycin 0.5 and 5 mM). 2APB did not diminish endothelial cell ATP-induced production of IP 3 nor e ect in vitro binding of [ 3 H]-IP 3 to an adrenal cortex binding protein. Capacitative Ca 2+ entry was also blocked by disruption of the actin cytoskeleton with cytochalasin (100 nM) while the initial Ca 2+ release phase was una ected. 4 Similarly to 2APB, xestospongin C (3 ± 10 mM) inhibited ATP-induced Ca 2+ release and capacitative Ca 2+ entry. Further, xestospongin C inhibited capacitative Ca 2+ entry induced by thapsigargin (1 mM) and ionomycin (0.5 mM). 5 The data are consistent with a mechanism of capacitative Ca 2+ entry in vascular endothelial cells which requires (a) IP 3 receptor binding and/or an event distal to the activation of the ER receptor and (b) a spatial relationship, dictated by the cytoskeleton, between Ca 2+ release and entry pathways.

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“…These results are similar to those obtained in platelets. For PGI2 synthesis, 16.2% of incorporated 3 H-AA is released from cultured vascular endothelial cell membranes; the rest is released from PI (3.4%), PE (3.5%) and PC (9.3%) 35) . These results show that both AA and EPA are metabolized to PGI2 or PGI3 through similar pathways in vascular endothelial cells, in which the PC of the blood membrane plays an important role.…”

Section: Phospholipid Subclasses In the Vascular Endothelial Cell Memmentioning

confidence: 99%

Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

Ohnishi

Saitō

2013

JAT

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The clinical efficacy of fish oil and high-purity eicosapentaenoic acid ethyl ester (hp-EPA-E) for treating cardiovascular disease (CVD) has been reported. Fish oil contains saturated and monounsaturated fatty acids that have pharmacological effects opposite to those of ω3 fatty acids (ω3). Moreover, ω3, such as EPA and docosahexaenoic acid (DHA), do not necessarily have the same metabolic and biological actions. This has obscured the clinical efficacy of ω3. Recently, the Japan EPA Lipid Intervention Study (JELIS) of hp-EPA-E established the clinical efficacy of EPA for CVD, and higher levels of blood EPA, not DHA, were found to be associated with a lower incidence of major coronary events. A significant reduction in the risk of coronary events was observed when the ratio of EPA to arachidonic acid (AA) (EPA/AA) was ＞0.75. Furthermore, the ratio of prostaglandin (

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Ca2+-dependent synthesis of prostaglandin I2 and mobilization of arachidonic acid from phospholipids in cultured endothelial cells permeabilized with saponin

Cited by 12 publications

References 56 publications

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Capacitative Ca²⁺ entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C

Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

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Ca2+-dependent synthesis of prostaglandin I2 and mobilization of arachidonic acid from phospholipids in cultured endothelial cells permeabilized with saponin

Cited by 12 publications

References 56 publications

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Capacitative Ca2+ entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C

Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

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Capacitative Ca²⁺ entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C