From nitric oxide to endothelial cytosolic Ca2+: a negative feedback control

Yao, Xiaoqiang; Huang, Yü

doi:10.1016/s0165-6147(03)00122-6

Cited by 45 publications

(42 citation statements)

References 23 publications

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“…Such hypothesis is in agreement with several previous observations on the properties of distinct AA-and NO-operated calcium channels in ECs (6,28). Here, the picture seems particularly complex.…”

Section: Discussionsupporting

confidence: 93%

“…Pretreatment of B-TECs with the membrane-permeable PKA inhibitory peptide myristoylated PKI [14][15][16][17][18][19][20][21][22] (10 minutes, 20 μmol/L) completely abolished AA-induced calcium entry in 99% of the cells tested (n = 84; Fig. 1; Table 1), suggesting a critical role of endogenous PKA in the activation of calcium signals by AA.…”

Section: Pka Is Required For Aa-induced Calcium Entry In B-tecsmentioning

confidence: 97%

“…Several groups, including ours, reported the ability of NO to open calcium channels in the plasma membrane of ECs (6,28). For these reasons, we investigated the effects of NO on Ca c signaling in B-TECs.…”

Section: No Triggers Calcium Entry and B-tec Migrationmentioning

confidence: 99%

“…NO mediates the function of many angiogenic factors and interferes with their expression. Furthermore, NO, through cyclic guanosine 3′,5′-monophosphate (cGMP)-dependent and cGMP-independent pathways, is able to regulate different types of calciumpermeable channels in ECs (1,2,4,(13)(14)(15)(16)(17)(18)(19)(20). In this context, we previously reported a crosstalk between arachidonateactivated calcium signals and NO metabolism (6).…”

Section: Introductionmentioning

confidence: 98%

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Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

Fiorio

Genova

Pupo

et al. 2010

Molecular Cancer Research

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We recently showed that arachidonic acid (AA) triggers calcium signals in endothelial cells derived from human breast carcinoma (B-TEC). In particular, AA-dependent Ca 2+ entry is involved in the early steps of tumor angiogenesis in vitro. Here, we investigated the multiple roles of the nitric oxide (NO) and cyclic AMP/protein kinase A (PKA) pathways in AA-mediated Ca 2+ signaling in the same cells. B-TEC stimulation with 5 μmol/L AA resulted in endothelial NO synthase (NOS) phosphorylation at Ser 1177 , and NO release was measured with the fluorescent NO-sensitive probe DAR4M-AM. PKA inhibition by the use of the membrane-permeable PKA inhibitory peptide myristoylated PKI 14-22 completely prevented both AA-and NOinduced calcium entry and abolished B-TEC migration promoted by AA. AA-dependent calcium entry and cell migration were significantly affected by both the NOS inhibitor N G -nitro-L-arginine methyl ester and the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide, suggesting that NO release is functionally involved in the signaling dependent on AA. Moreover, pretreatment with carboxyamidotriazole, an antiangiogenic compound that interferes with agonist-activated calcium entry, prevented AA-dependent B-TEC motility. Interestingly, even in the absence of AA, enhancement of the cyclic AMP/PKA pathway with the adenylyl cyclase activator forskolin evoked a calcium entry dependent on NOS recruitment and NO release. The functional relevance of AA-induced calcium entry could be restricted to tumor-derived endothelial cells (EC) because AA evoked a smaller calcium entry in normal human microvascular ECs compared with B-TECs, and even more importantly, it was unable to promote cell motility in wound healing assay. This evidence opens an intriguing opportunity for differential pharmacologic treatment between normal and tumor-derived human ECs.

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Section: Discussionsupporting

confidence: 93%

Section: Pka Is Required For Aa-induced Calcium Entry In B-tecsmentioning

confidence: 97%

Section: No Triggers Calcium Entry and B-tec Migrationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

Fiorio

Genova

Pupo

et al. 2010

Molecular Cancer Research

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“…Similar feedback inhibition has been well documented in vascular endothelial cells. [25][26][27] In this feedback mechanism, Ca 2+ influx would stimulate a nitric oxide-cGMP-PKG cascade, resulting in a negative feedback inhibition on Ca 2+ entry channels (i.e., heteromeric TRPV4-P2 channels in this case). The following sets of data support this notion: (1) ] i transients more sustained.…”

Section: Discussionmentioning

confidence: 99%

Protein Kinase G Inhibits Flow-Induced Ca2+ Entry into Collecting Duct Cells

Wong

Sun

et al. 2012

Journal of the American Society of Nephrology

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Intracellular calcium signaling regulates glomerular filtration barrier permeability: the role of the PKGIα‐dependent pathway

et al. 2016

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Edited by Lukas Alfons HuberPodocytes are dynamic polarized cells that lie on the surface of glomerular capillaries and comprise an essential component of the glomerular filtration barrier. Insulin provoked a sustained, approximately 70%, increase in intracellular calcium concentration in podocytes. RT-PCR revealed the presence of mRNA encoding sarco/endoplasmic reticulum calcium ATPase isoforms 1-3, and plasma membrane Ca 2+ pump (PMCA) isoforms 1,3,4; mRNA levels were depressed by the addition of insulin. Inhibitors of PMCA, and the Na + -Ca 2+ exchanger, increased podocyte permeability to albumin, induced dimerization of protein kinase G type I alpha (PKGIa), and activation of PKGIa-dependent signaling. These data suggest the involvement of calcium and PKGIa signaling in insulin-enhanced filtration barrier permeability in podocytes.

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From nitric oxide to endothelial cytosolic Ca2+: a negative feedback control

Cited by 45 publications

References 23 publications

Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

Protein Kinase G Inhibits Flow-Induced Ca2+ Entry into Collecting Duct Cells

Intracellular calcium signaling regulates glomerular filtration barrier permeability: the role of the PKGIα‐dependent pathway

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