Reach further, in an Open Access Journal Endocrinology, Diabetes & Metabolism Case Reports

ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2007) 14 P530 

The expression of the neuroprotective factor seladin-1 is up-regulated by thyroid hormones in human neuronal precursor cells, but not in mature neurons

Susanna Benvenuti1, Paola Luciani1, Ilaria Cellai1, Cristiana Deledda1, Riccardo Saccardi2, Serena Urbani2, Gabriella B Vannelli3, Fabio Francini4, Roberta Squecco4, Mario Serio1, Aldo Pinchera5 & Alessandro Peri1

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Thyroid hormones (TH) play a fundamental role during brain development by modulating the expression of different genes involved in neuronal differentiation, proliferation, migration, myelinization, and synapse formation. Seladin-1 (for SELective Alzheimer’s Disease INdicator-1) is a recently identified anti-apoptotic gene, which has been found to be down-regulated in brain regions affected by Alzheimer’s disease (AD). We hypothesized that seladin-1 might be a novel mediator of the effects of TH in the developing brain. Thus, in the present study we determined whether TH modulate the expression of seladin-1 in human neuronal precursors and/or in differentiated cells. Two different cell models were used: fetal human neuroepithelial cells (FNC) isolated previously from fetal olfactory epithelium; and human mesenchymal stem cells (hMSC), isolated from bone marrow, which have a demonstrated ability to differentiate into neurons. In our hands, hMSC were differentiated into neurons (hMSC-n), following previously established protocols. The neuronal phenotype was confirmed by the positivity for the specific markers nestin, glypican 4, necdin, neurofilament subunit L, neurofilament subunit M, neurite outgrowth-promoting protein, choline acetyltransferase, neuronal nuclei. Electrophysiological evaluation revealed the presence of inward Na and Ca currents typical of neuronal cells. In basal conditions, the amount of seladin-1 was significantly higher in undifferentiated cells than in mature neurons, as assessed by real-time RT-PCR. T3 and T4 (1 nM) significantly increased the amount of seladin-1 mRNA in both FNC (140% and 66% increase, respectively) and hMSC (61% and 16% increase, respectively), but not in hMSC-n. The amount of the protein, evaluated by Western blotting, changed accordingly. This is the first demonstration that TH stimulate the expression of seladin-1 in human neuronal precursors, but not in terminally differentiated neurons. These results suggest that this neuroprotective factor may play a prevalent role during brain development, together with other well-known TH-dependent factors.

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