D-117 | Thyroxine induces Neuro 2A cell differentiation and increases viability

D-117 | Thyroxine induces Neuro 2A cell differentiation and increases viability 150 150 SAN 2024 Annual Meeting

Neuroendocrinology and Neuroimmunology
Author: Mariana Elizabeth Troncoso | Email: troncoso.mariana@gmail.com


Mariana Troncoso1°2°, Flavia Neira, María Belén Sánchez,  María Cecilia Michel, Marta Soaje1°3°, Elisa Pietrobon1°3°, Luciana Viruel,  Esteban Lozano1°3°, Juan Pablo Mackern-Oberti1°3°, Susana Valdez1°2°

Insitituto de Medicina y Biología Experimental de Cuyo (IMBECU), CONICET, CCT – Mendoza.
Universidad Nacional de Cuyo, Facultad de Ciencias Exactas y Naturales.
Universidad Nacional de Cuyo, Facultad de Ciencias Médicas

Introduction: Neurogenesis, the process of generating new neurons, is crucial in embryonic development as in the adult brain. Thyroid hormones are key modulators of this process. Traditionally, the action of Triiodothyronine (T3) (biologically active hormone) has been studied, being less explored than the action of Thyroxine (T4) (non-genomic pathway). Objectives: to study the effect of T4 on the maturation, differentiation, and viability of the Neuro 2A cell line (Mouse Albino neuroblastoma). Methodology: Neuro 2A cells were cultured in DMEM supplemented with 10% fetal bovine serum (FBS). Treatments were conducted for 48 h with 5, 10, and 20 nM of T4 in DMEM containing 10% or 2% charcoal-stripped FBS (FBS CH). Retinoic acid (10 µM) was a positive control for neuronal differentiation. Results: T4 (5, 10, and 20 nM) in FBS CH 10% significantly (p < 0.01) increased neuronal differentiation without affecting viability relative to controls. In FBS CH 2%, T4 increased neuronal differentiation (p < 0.001) and viability (p < 0.001) relative to controls. In addition, 10 and 20 nM concentrations of T4 significantly (p < 0.01) induced the formation of differentiated neurons with complex morphology. Conclusion: T4 promotes neuronal differentiation in Neuro 2A cells and increases cell viability at low FBS concentrations. The relevance of this work lies in the fact that, in certain pathophysiological contexts, T4 activity could compensate or even modulate T3 action.

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