Expression of serotonin receptors in human fetal astrocytes and glioma cell lines: a possible role in glioma cell proliferation and migration

Merzak, Abderrahim; Koochekpour, Shahriar; Fillion, Marie‐Paule; Fillion, G.; Pilkington, Geoffrey J.

doi:10.1016/0169-328x(96)00058-7

Cited by 53 publications

(31 citation statements)

References 41 publications

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“…5-HT 2 receptors in glioma cells appear to regulate proliferation, migration, and invasion [46]. The 5-HT 2 receptor antagonists, ketanserin (10 − 6 M) and spiperone (10 − 6 M), blocked the stimulation of DNA synthesis by 5-HT indicating that the mitogenic activity of 5-HT is mediated through 5-HT 2 receptors.…”

Section: Discussionmentioning

confidence: 98%

Increased 5-HT2C receptor binding in the brain stem and cerebral cortex during liver regeneration and hepatic neoplasia in rats

Sulaiman

Joseph

Paulose

2007

Journal of the Neurological Sciences

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In the present study, serotonin 2C (5-HT(2C)) receptor binding parameters in the brainstem and cerebral cortex were investigated during liver generation after partial hepatectomy (PH) and N-nitrosodiethylamine (NDEA) induced hepatic neoplasia in male Wistar rats. The serotonin content increased significantly (p<0.01) in the cerebral cortex after PH and in NDEA induced hepatic neoplasia. Brain stem serotonin content increased significantly (p<0.05) after PH and (p<0.001) in NDEA induced hepatic neoplasia. The number and affinity of the 5-HT(2C) receptors in the crude synaptic membrane preparations of the brain stem showed a significant (p<0.001) increase after PH and in NDEA induced hepatic neoplasia. The number and affinity of 5-HT(2C) receptors increased significantly (p<0.001) in NDEA induced hepatic neoplasia in the crude synaptic membrane preparations of the cerebral cortex. There was a significant (p<0.01) increase in plasma norepinephrine in PH and (p<0.001) in NDEA induced hepatic neoplasia, indicating sympathetic stimulation. Thus, our results suggest that during active hepatocyte proliferation 5-HT(2C) receptor in the brain stem and cerebral cortex are up-regulated which in turn induce hepatocyte proliferation mediated through sympathetic stimulation.

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Section: Discussionmentioning

confidence: 98%

Increased 5-HT2C receptor binding in the brain stem and cerebral cortex during liver regeneration and hepatic neoplasia in rats

Sulaiman

Joseph

Paulose

2007

Journal of the Neurological Sciences

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“…Alternatively, RA and 5-HT 2 -mediated serotonergic signaling could exert opposing effects on common processes, such as cell proliferation. The latter possibility is supported by evidence that 5-HT acts as a mitogenic signal for craniofacial mesenchymal cells, tumor cell lines, and other cell types, mediated by 5-HT 2B receptors (Buznikov et al 2001;Choi et al 1994;Choi et al 1997;Kellermann et al 1998;Loric et al 1995;Nebigil et al 1998), the 5-HT transporter (Fanburg and Lee 1997;Lee et al 1998;Lee et al 1999;Lee et al 1991), and other 5-HT receptors (Edgar et al 1999;Merzak et al 1996;Pakala et al 1999;Pizzinat et al 1999;Takuwa et al 1989). On the contrary, at certain concentrations, RA negatively regulates proliferation of migrating neural crest cells (Salvarezza and Rovasio 1997), tumor cell lines, and other cell types (Blumentrath et al 2001;Campione-Piccardo et al 1985;Kishi et al 2001;Salvarezza and Rovasio 1997); thus, we asked whether RA and 5-HT receptor agonists have distinct effects on cell proliferation in the context of E-M interactions during early development.…”

Section: Introductionmentioning

confidence: 92%

Opposing regulation of cell proliferation by retinoic acid and the serotonin 2B receptor in the mouse frontonasal mass

Bhasin

LaMantia

Lauder

2004

Anatomy and Embryology

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Development of the frontonasal mass (FNM), branchial arches, heart, and limbs depends on neural crest-mediated epithelial-mesenchymal (E-M) interactions. Teratogenesis by retinoic acid (RA) or blockade of serotonergic (5-HT) signaling by the pan-5-HT(2) receptor antagonist, ritanserin, perturbs development of these embryonic structures. In both cases, resulting phenotypes include forebrain and olfactory placode anomalies, malformations of the face, eye and lens, as well as posterior neural tube and cardiac defects. Similar sites of malformations, together with the presence of RA response elements in the 5-HT(2B) receptor promoter, have led to the suggestion that a negative regulatory relationship may exist between RA and 5-HT(2)-mediated 5-HT signaling at sites of E-M interaction (Choi et al. 1997); however, another possibility is that RA and 5-HT act independently as opposing signals to regulate development of common embryonic targets. Together with recent evidence for opposite effects on chondrogenic differentiation in hindlimb micromass cultures (Bhasin et al. 2003a), results of the present study raise the possibility that these pathways may act as opposing signals for common targets in the mouse embryo. The RA receptors, co-factors and metabolic enzymes, and 5-HT(2B) receptors were found to be are coordinately expressed at sites of E-M interaction, including the FNM, in the embryonic day (E)10.5 mouse. Cell proliferation experiments using [(3)H]thymidine incorporation demonstrated that RA or activation of 5-HT(2B) receptors caused opposite effects in FNM explants, namely stimulation or inhibition of cell proliferation, respectively, 5-HT(2B) receptor activation did not appreciably alter patterning in FNM explants. While RA has been shown to regulate lateral patterning in the FNM (LaMantia et al. 2000), 5-HT(2B) receptor activation did not alter patterning in FNM explants. Quantification of 5-HT(2B) receptor transcripts by real-time PCR provided no evidence of negative regulation of 5-HT(2B) receptor expression by RA in FNM explants, although preliminary studies using in situ hybridization had suggested that this was a possibility in both explants and RA teratogenized embryos. Future studies using quantitative PCR may still show this to be the case in teratogenized embryos. Together with the finding of coordinate expression of 5-HT(2B )receptors and RA signaling molecules, results of the present study suggest that RA, and 5-HT mediated by 5-HT(2B )receptors, may act as opposing signals to regulate cell proliferation during craniofacial development in the mouse embryo.

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“…The serotonin (5-HT) 5-HT 2B receptor regulates morphogenesis in mouse cranial neural crest and myocardiac cells (Choi et al 1997;Bhasin et al 2004), and it plays a major role in normal and abnormal heart function during adulthood (Rothman et al 2000; Maroteaux cultures of mouse astrocytes together with 5-HT 2A and 5-HT 2C receptors as well as non-5-HT 2 receptors and the serotonin transporter (Deecher et al 1993;Merzak et al 1996;Hirst et al 1998;Sandén et al 2000;Kong et al 2002). However, in astrocyte cultures that have been treated with dibutyryl cyclic AMP (dBcAMP) to enhance differentiation (Meier et al 1991), reverse transcription-polymerase chain reaction (RT-PCR) has shown that the serotonin transporter is not expressed and that the 5-HT 2B receptor is a major 5-HT 2 receptor (Kong et al 2002; see also below).…”

Section: Introductionmentioning

confidence: 97%

Fluoxetine-mediated 5-HT2B receptor stimulation in astrocytes causes EGF receptor transactivation and ERK phosphorylation

Zhang

et al. 2008

Psychopharmacology

100

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ERK(1/2) phosphorylation was abolished by SB204741, a universal 5-HT(2) receptor antagonist, and in 5-HT(2B) receptor-depleted cells, but unaffected by 5-HT(2A) or 5-HT(2C) receptor antagonists (M100907 and SB242084). Phosphorylation of ERK(1/2) and EGFRs was abolished by AG 1478, an inhibitor of EGFR tyrosine kinases, and GM 6001, an inhibitor of Zn-dependent metalloproteinases, suggesting growth factor "shedding" and transactivation of EGFRs. Chelation of [Ca(2+)](i) or PKC inhibition with GF 109203X abrogated ERK(1/2) phosphorylation. Up-regulated mRNA and protein expression of c-fos and fosB was abolished by SB204741, AG1478, and by U0126, an inhibitor of ERK phosphorylation by MAP kinase/ERK kinase.

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Expression of serotonin receptors in human fetal astrocytes and glioma cell lines: a possible role in glioma cell proliferation and migration

Cited by 53 publications

References 41 publications

Increased 5-HT2C receptor binding in the brain stem and cerebral cortex during liver regeneration and hepatic neoplasia in rats

Increased 5-HT2C receptor binding in the brain stem and cerebral cortex during liver regeneration and hepatic neoplasia in rats

Opposing regulation of cell proliferation by retinoic acid and the serotonin 2B receptor in the mouse frontonasal mass

Fluoxetine-mediated 5-HT2B receptor stimulation in astrocytes causes EGF receptor transactivation and ERK phosphorylation

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