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Serotonin and its transporter on proliferation of fetal heart cells
Author(s) -
Sari Youssef,
Zhou Feng C.
Publication year - 2003
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2003.10.002
Subject(s) - serotonin , serotonin transporter , endocrinology , medicine , heart development , serotonergic , biology , fetus , cell growth , heart cells , 5 ht receptor , microbiology and biotechnology , chemistry , myocyte , receptor , embryonic stem cell , biochemistry , pregnancy , genetics , gene
Besides neuronal transmission, serotonin (5‐HT) also acts as a trophic signal during the development of the central nervous and neural crest systems. In this study, we report that in addition to trophic effect, 5‐HT increases the proliferation of fetal heart cells. We showed for the first time that the cultured heart cells, express serotonin transporter (5‐HTT), which confirmed the previously observed accumulation of 5‐HT in developing heart. The influence of 5‐HT on developing heart cells is studied throughout the dosage. We found that 5‐HT concentration at physiological level, 4 μM, permits an optimal proliferation of heart cells as indicated by the number of 5‐bromo‐deoxyuridine immunoreactive (BrdU‐im) cells and myosin heavy chain immunoreactive cells (MF20‐im); fluctuation towards either concentrations reduce the proliferation. We hypothesized that 5‐HTT plays a role in the heart development. Our study indicated that the blockade of 5‐HT uptake by paroxetine decreased the number of BrdU‐im cells and MF20‐im cells. These data indicate a role of 5‐HT and 5‐HTT on heart development. Abnormal 5‐HT level or misuse of 5‐HT uptake blocker may alter the heart development.