P2Y1 and P2Y2 Receptor-Operated Ca2+ Signals in Primary Cultures of Cardiac Microvascular Endothelial Cells

Moccia, Francesco; Baruffi, Silvana; Spaggiari, S.; Coltrini, Daniela; Berra‐Romani, Roberto; Signorelli, Silvia; Castelli, Loretta; Taglietti, Vanni; Tanzi, Franco

doi:10.1006/mvre.2001.2306

Cited by 43 publications

(47 citation statements)

References 28 publications

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“…We found that in nominally Ca 2 þ -free solution, the maximally effective concentrations of bradykinin, ATP and 2-methylthio ATP induced a transient elevation of intracellular Ca 2 þ . In addition, ATP, a non-selective agonist for P2Y receptors, elicited a higher signal than 2-methylthio ATP, whose effects are probably mediated by P2Y 1 receptors, as described previously by Moccia et al (2001). Melatonin had a similar effect on bradykinin and 2-methylthio ATP-induced Ca 2 þ responses in reducing the peak response; however, with 2-methylthio ATP, the onset of the Ca 2 þ response was delayed.…”

supporting

confidence: 77%

Melatonin inhibits nitric oxide production by microvascular endothelial cells in vivo and in vitro

Silva

Tamura

Macedo

et al. 2007

British J Pharmacology

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Background and purpose: We have previously shown that melatonin inhibits bradykinin-induced NO production by endothelial cells in vitro. The purpose of this investigation was to extend this observation to an in vivo condition and to explore the mechanism of action of melatonin. Experimental approach: RT-PCR assays were performed with rat cultured endothelial cells. The putative effect of melatonin upon arteriolar tone was investigated by intravital microscopy while NO production by endothelial cells in vitro was assayed by fluorimetry, and intracellular Ca 2 þ measurements were assayed by confocal microscopy. Key results: No expression of the mRNA for the melatonin synthesizing enzymes, arylalkylamine N-acetyltransferase and hydroxyindole-O-methyltransferase, or for the melatonin MT 2 receptor was detected in microvascular endothelial cells. Melatonin fully inhibited L-NAME-sensitive bradykinin-induced vasodilation and also inhibited NO production induced by histamine, carbachol and 2-methylthio ATP, but did not inhibit NO production induced by ATP or a, b-methylene ATP. None of its inhibitory effects was prevented by the melatonin receptor antagonist, luzindole. In nominally Ca 2 þ -free solution, melatonin reduced intracellular Ca 2 þ mobilization induced by bradykinin (40%) and 2-methylthio ATP (62%) but not Ca 2 þ mobilization induced by ATP. Conclusions and implications:We have confirmed that melatonin inhibited NO production both in vivo and in vitro. In addition, the melatonin effect was selective for some G protein-coupled receptors and most probably reflects an inhibition of Ca 2 þ mobilization from intracellular stores.

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supporting

confidence: 77%

Melatonin inhibits nitric oxide production by microvascular endothelial cells in vivo and in vitro

Silva

Tamura

Macedo

et al. 2007

British J Pharmacology

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“…20,[24][25][26] With reference to the literature, 100 µM ATP and UTP, were applied to VMFs throughout this study so that the Ca 2+ signaling properties could be investigated based on the maximal responses generated. Similar efficacies of [Ca 2+ ] i responses elicited by ATP and UTP were seen in VMFs, and clear Ca 2+ influx components were demonstrated in the presence of both agonists.…”

Section: Discussionmentioning

confidence: 99%

P2Y2 Receptor-Mediated Ca2+ Signaling and Spontaneous Ca2+ Releases in Human Valvular Myofibroblasts

et al. 2008

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“…The procedure for cell isolation has been described previously [20,21], and is very similar to the procedure originally developed by Nishida et al [22]. Adult Wistar rats (250-350 g) were anaesthetized with ether, and the heart was rapidly excised and perfused in retrograde with Dulbecco's modified Eagle's Medium (DMEM) saturated with an O # \CO # mixture (19 : 1).…”

Section: Isolation and Culture Of Cmecsmentioning

confidence: 99%

Ca2+ uptake by the endoplasmic reticulum Ca2+-ATPase in rat microvascular endothelial cells

Moccia

Berra‐Romani

Baruffi

et al. 2002

Biochemical Journal

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In non-excitable cells, many agonists increase the intracellular Ca# + concentration ([Ca# + ] i ) by inducing an inositol 1,4,5-trisphosphate (IP $ )-mediated Ca# + release from the intracellular stores. Ca# + influx from the extracellular medium may then sustain the Ca# + signal. [Ca# + ] i recovers its resting level as a consequence of Ca# + -removing mechanisms, i.e. plasma-membrane Ca# + -ATPase (PMCA) pump, Na + \Ca# + exchanger (NCX) and sarco-endoplasmic reticulum Ca# + -ATPase (SERCA) pump. In a study performed in pancreatic acinar cells, evidence has been provided suggesting that, during the decay phase of the agonistevoked Ca# + transients, the Ca# + concentration within the intracellular stores remains essentially constant [Mogami, Tepikin and Petersen (1998) EMBO J. 17, [435][436][437][438][439][440][441][442]. It was therefore hypothesized that, in such a situation, intracellular Ca# + is not only picked up by the SERCA pump, but is also newly released through IP $ -sensitive Ca# + channels, with the balance between these two processes being approximately null. The main aim of the present work was to test this hypothesis by a different experimental approach. Using cardiac microvascular endothelial cells, we found that inhibition of the SERCA pump has no effect on the time course of agonist-evoked Ca# + transients. This

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P2Y1 and P2Y2 Receptor-Operated Ca2+ Signals in Primary Cultures of Cardiac Microvascular Endothelial Cells

Cited by 43 publications

References 28 publications

Melatonin inhibits nitric oxide production by microvascular endothelial cells in vivo and in vitro

Melatonin inhibits nitric oxide production by microvascular endothelial cells in vivo and in vitro

P2Y2 Receptor-Mediated Ca2+ Signaling and Spontaneous Ca2+ Releases in Human Valvular Myofibroblasts

Ca2+ uptake by the endoplasmic reticulum Ca2+-ATPase in rat microvascular endothelial cells

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