Arachidonic acid regulates two Ca2+ entry pathways via nitric oxide

Watson, Eileen L.; Jacobson, Kerry L.; Singh, J.; DiJulio, Dennis H.

doi:10.1016/s0898-6568(03)00102-5

Cited by 36 publications

(50 citation statements)

References 55 publications

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“…The mechanisms underlying this phenomenon are still unclear. Some authors suggest that NO either directly or indirectly acts as a messenger downstream of AA to inhibit SOCE (70)(71)(72). Another hypothesized mechanism is a direct interaction between AA and store-operated channel or an alteration of the lipid environment by AA (70).…”

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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“…Some reports have shown that AA and PPARs stimulate NO production in many tissues and cells (7,13,15,19,21,22). AA has been reported to stimulate cGMP accumulation via NO production in vascular smooth muscle cells (9).…”

Section: Effects Of Bay-60-7550 (A Pde2 Inhibitor) On Ca 2ϩ -Regulatementioning

confidence: 99%

A PKG inhibitor increases Ca²⁺-regulated exocytosis in guinea pig antral mucous cells: cAMP accumulation via PDE2A inhibition

Tanaka

Harada

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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In antral mucous cells, acetylcholine (ACh, 1 M) activates Ca 2ϩ -regulated exocytosis, consisting of an initial peak that declines rapidly (initial transient phase) followed by a second slower decline (late phase) lasting during ACh stimulation. The addition of 8-bromo-cGMP (8-BrcGMP) enhanced the initial phase, which was inhibited by the protein kinase G (PKG) inhibitor guanosine 3=,5=-cyclic monophosphorothoiate, ␤-phenyl-1,N 2 -etheno-8-bromo, Rp-isomer, sodium salt (Rp-8-BrPETcGMPS, 100 nM). However, Rp-8-BrPETcGMPS produced a delayed, but transient, increase in the exocytotic frequency during the late phase that was abolished by a protein kinase A (PKA) inhibitor (PKI-amide), suggesting that Rp-8-BrPETcGMPS accumulates cAMP. The cGMP-dependent phosphodiesterase 2 (PDE2), which degrades cAMP, may exist in antral mucous cells. The PDE2 inhibitor BAY-60-7550 (250 nM) mimicked the effect of Rp-8-BrPETcGMPS on ACh-stimulated exocytosis. Measurement of the cGMP and cAMP contents in antral mucosae revealed that ACh stimulates the accumulation of cGMP and that BAY-60-7550 accumulates cAMP similarly to Rp-8-BrPETcGMPS during ACh stimulation. Analyses of Western blot and immunohistochemistry demonstrated that PDE2A exists in antral mucous cells. In conclusion, Rp-8-BrPETcGMPS accumulates cAMP by inhibiting PDE2 in AChstimulated antral mucous cells, leading to the delayed, but transient, increase in the frequency of Ca 2ϩ -regulated exocytosis. PDE2 may prevent antral mucous cells from excessive mucin secretion caused by the cAMP accumulation.acetylcholine; guanosine 3=,5=-cyclic monophosphate; adenosine 3=,5=-cyclic monophosphate; gastric; mucin secretion GASTRIC MUCINS, WHICH ARE high-molecular-weight glycoproteins that protect the gastric mucosa from acid-peptic injury, are stored in intracellular granules and secreted to the lumen by Ca 2ϩ -regulated exocytosis. Ca 2ϩ -regulated exocytosis in antral mucous cells consists of three biochemically distinct steps: docking, priming, and fusion. The priming step is regulated by ATP, and the fusion step is regulated by Ca 2ϩ (12,20,23). In antral mucous cells, Ca 2ϩ -regulated exocytosis has characteristic features of frequency: an initial peak that declines rapidly (initial phase or initial transient phase) followed by a second slower decline (late phase) lasting during acetylcholine (ACh) stimulation. The initial phase, which is transient and has a high frequency of exocytotic events, is caused by an immediate fusion of the primed granules (the pool of releasable granules), and the late phase, which has a low frequency of exocytotic events, is caused by a fusion of granules that are in the process of priming (10).In antral mucous cells, Ca 2ϩ -regulated exocytosis is activated by ACh and is modulated by many substances, such as cAMP, cGMP, arachidonic acid (AA), and intracellular Cl Ϫ (3, 4, 10, 11, 14 -18). An accumulation of cAMP, which accelerates the priming step and the fusion step, also significantly increases the frequency of the initial phase in Ca 2ϩ -regulat...

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“…Hawkins et al [188] studied redox mediated activation of STIM1 and found that oxidative stress leads to gluthationylation of STIM1's cysteine 56, triggering STIM1 oligomerization and punctae [171][172][173][174][175][176][177][180][181][182][183][184][185][186]189,[192][193][194][195][203][204][205][206][207][208][209][210][211][212][213][214][215][216][217][218] BSO, buthionine sulfoximine; DEANO, 2-(N,N-diethylamino)diazenolate-2-oxide; FRTL-5, fischer rat thyroid low serum 5%; GEA3162, 1,2,3,4,-oxatriazolium, 5-amino-3-(3,4-dichlorophenyl)-chloride; HEK, human embryonic kidney; IP3R, IP3 receptor; Jurkat, human leukemic T cell line; MEF, mouse embryonic fibroblasts; RBL, rat basophilic leukemia; RyR, ryanodine receptor; SH-SY5Y, human neuroblastoma cell line; SNP, sodium nitroprusside; tBHP, tert-butylhydroperoxide.…”

Section: Reactive Oxygen Species Effects On Soce and Crac/orai Channelsmentioning

confidence: 99%

“…Inhibition of SOCE by an NO donor was also reported by Watson at al. [218]. A summary of redox regulation of CRAC/Orai channels is given in Table 4.…”

Section: Reactive Nitrogen Species Effects On Soce and Crac/orai Chanmentioning

confidence: 99%

Redox regulation of calcium ion channels: Chemical and physiological aspects

et al. 2011

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a b s t r a c tReactive oxygen species (ROS) are increasingly recognized as second messengers in many cellular processes. While high concentrations of oxidants damage proteins, lipids and DNA, ultimately resulting in cell death, selective and reversible oxidation of key residues in proteins is a physiological mechanism that can transiently alter their activity and function. Defects in ROS producing enzymes cause disturbed immune response and disease.Changes in the intracellular free Ca 2+ concentration are key triggers for diverse cellular functions. Ca 2+ homeostasis thus needs to be precisely tuned by channels, pumps, transporters and cellular buffering systems. Alterations of these key regulatory proteins by reversible or irreversible oxidation alter the physiological outcome following cell stimulation. It is therefore necessary to understand which proteins are regulated and if this regulation is relevant in a physiological-and/or pathophysiological context. Because ROS are inherently difficult to identify and to measure, we first review basic oxygen redox chemistry and methods of ROS detection with special emphasis on electron paramagnetic resonance (EPR) spectroscopy. We then focus on the present knowledge of redox regulation of Ca 2+ permeable ion channels such as voltage-gated (CaV) Ca 2+ channels, transient receptor potential (TRP) channels and Orai channels.© 2011 Elsevier Ltd. All rights reserved. Basic redox chemistry of oxygenMany chemical processes are linked to the exchange of electrons between two or more molecular entities. The transfer of one (or more) electron(s) is associated with oxidation (loss of electron) and reduction (gain of electron) of the components. Such reactions are also known as redox reactions. The processes of reactive oxygen species (ROS) formation and elimination are exclusively of redox nature.Molecular oxygen is the precursor of all ROS. It contains two unpaired electrons in separate (antibonding) orbitals in its outer electron sphere and is thus, by definition, a radical. Radicals have at least one unpaired electron in their orbital system and usually show high reactivity; transition metal ions also may have unpaired electrons, but are not called radicals. Although having radical character, molecular oxygen is chemically rather inert (luckily!), because high * Corresponding authors at: Institut für Biophysik, Gebäude 58, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: +49 6841 1626453; fax: +49 6841 1626060.E-mail addresses: ivan.bogeski@uks.eu (I. Bogeski), barbara.niemeyer@uks.eu (B.A. Niemeyer).

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Arachidonic acid regulates two Ca2+ entry pathways via nitric oxide

Cited by 36 publications

References 55 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

A PKG inhibitor increases Ca²⁺-regulated exocytosis in guinea pig antral mucous cells: cAMP accumulation via PDE2A inhibition

Redox regulation of calcium ion channels: Chemical and physiological aspects

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Arachidonic acid regulates two Ca2+ entry pathways via nitric oxide

Cited by 36 publications

References 55 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

A PKG inhibitor increases Ca2+-regulated exocytosis in guinea pig antral mucous cells: cAMP accumulation via PDE2A inhibition

Redox regulation of calcium ion channels: Chemical and physiological aspects

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A PKG inhibitor increases Ca²⁺-regulated exocytosis in guinea pig antral mucous cells: cAMP accumulation via PDE2A inhibition