[The 5-HT2B receptor: a main cardio-pulmonary target of serotonin].

Abstract

In agreement with previous data in the literature, our results indicate that serotonin, a monoamine neurotransmitter, can also regulate cell proliferation, cell movements and cell differentiation. We have recently shown that serotonin is required for embryonic heart development. Genetic ablation of the 5-HT2B receptor leads to partial embryonic and postnatal lethality with abnormal heart development. Similar molecular mechanisms seem to be involved in adult cardiomyocytes since mutant mice surviving to adulthood display a dilated cardiomyopathy. Furthermore this receptor appears to be involved in survival of cardiomyocytes. The 5-HT2B receptor is also implicated in systemic hypertension. Furthermore, mice with pharmacological or genetic ablation of 5-HT2B receptor are totally resistant to hypoxia-induced pulmonary hypertension, indicating that this receptor is regulating the pathologic vascular proliferation leading to this disease. Underlying mechanisms are still to be discovered.

• Authors: Nelly Etienne, Bérénice Schaerlinger, Fabrice Jaffré, Luc Maroteaux
• Journal: Journal de la Societe de biologie (J Soc Biol) Vol. 198 Issue 1 Pg. 22-9 ( 2004) ISSN: 1295-0661 [Print] France
• Vernacular Title: Le récepteur 5-HT2B: une cible privilégiée de la sérotonine au niveau cardio-pulmonaire.
• PMID: 15146952 (Publication Type: Journal Article, Review)

Chemical References

• Receptor, Serotonin, 5-HT2B
• TGFB1 protein, human
• Tgfb1 protein, mouse
• Tgfb1 protein, rat
• Transforming Growth Factor beta
• Transforming Growth Factor beta1
• Fenfluramine
• Serotonin
• Pancreatic Elastase

Topics

• Adult
• Animals
• Cardiomyopathy, Dilated (genetics, metabolism)
• Cell Survival
• Fenfluramine (adverse effects, pharmacokinetics)
• Fetal Heart (metabolism)
• Genes, Lethal
• Genetic Predisposition to Disease
• Heart Defects, Congenital (embryology, genetics)
• Humans
• Hypertension (genetics)
• Hypertension, Pulmonary (etiology)
• Hypoxia (complications)
• Mice
• Mice, Knockout
• Mice, Transgenic
• Muscle, Smooth, Vascular (cytology, drug effects)
• Myocytes, Cardiac (cytology, metabolism)
• Organ Specificity
• Pancreatic Elastase (physiology)
• Pulmonary Artery (pathology)
• Rats
• Receptor, Serotonin, 5-HT2B (deficiency, genetics, physiology)
• Serotonin (physiology)
• Transforming Growth Factor beta (physiology)
• Transforming Growth Factor beta1