Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Bostel, Sébastien; Malo, Michel; Rouzaire‐Dubois, Béatrice; Dubois, Jean‐Marc

doi:10.1007/s00424-002-0786-0

Cited by 9 publications

(7 citation statements)

References 34 publications

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“…The discrepancy between our in vitro findings and reported in vivo findings may be due to one of several factors: In vivo, the ductus is exposed to shear stresses that were not considered in our in vitro model; caffeine might interact with shearrelated signaling (27). Caffeine may also act at some site distant from the ductus, altering the production of circulating substances that might affect ductus contractility.…”

Section: Clyman and Romancontrasting

confidence: 65%

The Effects of Caffeine on the Preterm Sheep Ductus Arteriosus

Clyman

Roman

2007

Pediatr Res

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Caffeine and other methyl xanthines are widely used in the neonatal period. A recent, randomized, placebo-controlled, multicenter trial found that infants who were randomly assigned to caffeine treatment had less need for pharmacologic and/or surgical closure of a patent ductus arteriosus (PDA). We hypothesized that the decreased need for pharmacologic and surgical closure of the PDA after caffeine treatment might be due to a direct effect of caffeine on ductus contractility. We examined preterm fetal lamb ductus arteriosus (from 24 fetuses, 105 Ϯ 4 d of gestation, term ϭ 147 d), in vitro to determine the direct effects of caffeine on the isometric tension of the ductus arteriosus. Caffeine (0.003-0.3 mM) had no direct effect on ductus arteriosus tension, nor did it affect the contractile response of the ductus arteriosus to increasing oxygen concentrations. Caffeine's lack of effect was observed in both the presence and absence of indomethacin and N g -nitro-L-arginine methyl ester (L-NAME) (inhibitors of prostaglandin and nitric oxide production). In conclusion, we found no evidence of a direct effect of therapeutic caffeine concentrations on ductus contractility. ) (1-10), in vivo studies suggest that postnatal constriction is primarily determined by a shift in the balance between oxygen (a ductus constrictor) and prostaglandins and nitric oxide (ductus dilators) (11,12). Alterations in antenatal glucocorticoid concentrations and postnatal pulmonary vascular resistance also play roles in in vivo ductus constriction (13,14).Recently, a randomized, placebo-controlled, multicenter trial was performed to evaluate the effects of caffeine administration in preterm infants (15). Infants were enrolled in the trial during the first 10 d after birth, and the primary goal of the study was to evaluate the long-term effects of caffeine on neurodevelopmental outcome. An unexpected finding of the study was that infants who were randomly assigned to caffeine treatment had less need for pharmacologic and/or surgical closure of a PDA.Caffeine has been found to directly affect several of the signaling molecules that are involved in ductus constriction: it increases cAMP by inhibiting cyclic nucleotide phosphodiesterase (16); it releases Ca 2ϩ from the endoplasmic reticulum by binding to the ryanodine receptor (17); it inhibits both prostaglandin production (18) and activity (19) and inhibits adenosine activity by binding to its receptors (20). At therapeutic concentrations, caffeine's effects appear to be due primarily to antagonism of the adenosine receptor (21).In this study, we hypothesized that the decreased need for pharmacologic and surgical closure of the PDA after caffeine treatment might be due to a direct effect of caffeine on ductus contractility. To examine this hypothesis, we studied the effects of caffeine on the isolated preterm fetal sheep ductus arteriosus. METHODSPreterm fetal lambs (mixed Western breed: 105 Ϯ 4 d of gestation, term ϭ 147) were delivered by cesarean section and anesthetized with keta...

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Section: Clyman and Romancontrasting

confidence: 65%

The Effects of Caffeine on the Preterm Sheep Ductus Arteriosus

Clyman

Roman

2007

Pediatr Res

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“…In contrast to the present results showing that NPPB increased the percentage of cells in S phase, it has been shown in cervical cancer cells (Shen et al, 2000) and nasopharyngeal carcinoma cells (Chen et al, 2002) that this agent arrested cells in G0/G1 phase. This may be due to cell type differences and to the fact that NPPB is a nonspecific Cl − channel blocker, which efficiently blocks K + channels involved in cell volume regulation (Bostel et al, 2002). Consequently, and depending on cell types and/or experimental conditions, differential expressions of K + and Cl − channels during the cell cycle (e.g., Takahashi et al, 1993; Doroshenko et al, 2001; Ouadid‐Ahidouch et al, 2001; Chen et al, 2002) may control the cell cycle progression differentially.…”

Section: Discussionmentioning

confidence: 99%

Cell size‐proliferation relationship in rat glioma cells

Rouzaire‐Dubois

Malo

Milandri

et al. 2003

Glia

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The homeostasis of the central nervous system is highly controlled by glial cells and is dramatically altered in the case of glioma. In this respect, the complex connection between cell size and division is of particular importance and needs clarifying. In order to investigate this connection, cell number and volume were measured in C6 rat glioma cells under different experimental conditions, including continuous cell culture, Cl- channel blockade, and anisotonicity, and in the presence of an inhibitory conditioned medium collected from cell cultures or in a medium containing a low level of fetal calf serum. The rate of cell proliferation changed with cell volume in a bell-shaped manner, so that it is optimal within a cell volume window and appears to be controlled by low and high cell size checkpoints. The cell size-proliferation relationship can be defined by Boltzmann-like equations, which may reflect the effects of macromolecular crowding on proteins controlling the cell cycle progression. Altogether, these observations indicate that glioma cell proliferation is controlled predominantly but not exclusively by cell size-dependent mechanisms.

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“…An intriguing aspect of the biology of malignant gliomas is that it is the same ion transport mechanisms that normally control homeostatic processes such as the regulation of cell volume (Bostel et al, 2002), proliferation and differentiation (Pancrazio et al, 1999), that often become part of the pathogenesis and malignancy of these tumours. The expression profile of ion channels is known to be profoundly altered in glial tumour cells (Bordey and Sontheimer, 1998;Bubien et al, 1999;Ranson and Sontheimer, 2001;Olsen and Sontheimer, 2004).…”

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confidence: 99%

hERG1 channels are overexpressed in glioblastoma multiforme and modulate VEGF secretion in glioblastoma cell lines

et al. 2005

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Recent studies have led to considerable advancement in our understanding of the molecular mechanisms that underlie the relentless cell growth and invasiveness of human gliomas. Partial understanding of these mechanisms has (1) improved the classification for gliomas, by identifying prognostic subgroups, and (2) pointed to novel potential therapeutic targets. Some classes of ion channels have turned out to be involved in the pathogenesis and malignancy of gliomas. We studied the expression and properties of K þ channels in primary cultures obtained from surgical specimens: human ether a gò-gò related (hERG)1 voltage-dependent K þ channels, which have been found to be overexpressed in various human cancers, and human ether a gò-gò-like 2 channels, that share many of hERG1's biophysical features. The expression pattern of these two channels was compared to that of the classical inward rectifying K þ channels, IRK, that are widely expressed in astrocytic cells and classically considered a marker of astrocytic differentiation. In our study, hERG1 was found to be specifically overexpressed in high-grade astrocytomas, that is, glioblastoma multiforme (GBM). In addition, we present evidence that, in GBM cell lines, hERG1 channel activity actively contributes to malignancy by promoting vascular endothelial growth factor secretion, thus stimulating the neoangiogenesis typical of high-grade gliomas. Our data provide important confirmation for studies proposing the hERG1 channel as a molecular marker of tumour progression and a possible target for novel anticancer therapies.

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Calcium and voltage-dependent alterations of cell volume in neuroblastoma×glioma hybrid NG108-15 cells

Cited by 9 publications

References 34 publications

The Effects of Caffeine on the Preterm Sheep Ductus Arteriosus

The Effects of Caffeine on the Preterm Sheep Ductus Arteriosus

Cell size‐proliferation relationship in rat glioma cells

hERG1 channels are overexpressed in glioblastoma multiforme and modulate VEGF secretion in glioblastoma cell lines

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