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ORIGINAL RESEARCH article
Front. Cell Dev. Biol.
Sec. Stem Cell Research
Volume 13 - 2025 |
doi: 10.3389/fcell.2025.1551090
Prolactin drives cortical neuron maturation and dendritic development during murine embryonic stem cell differentiation
Provisionally accepted
Omar Martínez 1
Daniela Colin-Lagos 1
Ximena Ramirez-Meza 1 Alejandra Castilla 2 Georgina Hernandez-Montes 2
Eliezer Flores-Garza 3 Alejandro Lopez-Saavedra 4
Daniela Avila-González 1 Alejandro Martinez-Juarez 1
Anayansi Molina-Hernández 1
Néstor E Diaz-Martínez 5
Wendy Portillo 2
Nestor Fabian Diaz 1*- 1 Instituto Nacional de Perinatología (INPER), Mexico City, México, Mexico
- 2 National Autonomous University of Mexico, México City, México, Mexico
- 3 Imperial College London, London, England, United Kingdom
- 4 Monterrey Institute of Technology and Higher Education (ITESM), Monterrey, Nuevo León4, Mexico
- 5 CONACYT Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco (CIATEJ), Guadalajara, Jalisco, Mexico
Prolactin (PRL) is a multifunctional hormone involved in various physiological processes, yet its role in neurodevelopment remains poorly understood. This study investigates PRL's regulatory influence on early corticogenesis, focusing on its effects on neuronal and astrocyte differentiation during neural development. We employed an in vitro differentiation protocol to derive cortical neurons from mouse embryonic stem cells (mESCs). Prolactin receptor (PRLr) expression was detected in pluripotent stem cells, neural stem cells (NSCs), immature neurons, and mature neurons, displaying progressive dynamics throughout differentiation. PRL treatments during early neural differentiation significantly increased β-tubulin III+ immature neuron populations, enhancing neuronal survival without affecting NSC proliferation. Early PRL exposure also elevated Tbr1+ and NeuN+ populations, promoted dendritic complexity, and advanced neuronal maturation. In contrast, PRL treatments during late neural differentiation were ineffective. Additionally, PRL delayed protoplasmic astrocyte maturation without altering the total number of astrocytes. These findings demonstrate PRL's critical role as a regulator of early corticogenesis, influencing neuronal survival, dendritic complexity, and astrocyte maturation. This study highlights PRL's potential as a key factor in neurodevelopment and provides insights into its contribution to corticogenesis, with broader implications for understanding hormonal regulation in neural differentiation and maturation.
Keywords: Prolactin1, Prolactin receptor2, Cortical neurons3, Neural stem cells4, pluripotent stem cells5
Received: 24 Dec 2024; Accepted: 04 Feb 2025.
Copyright: © 2025 Martínez, Colin-Lagos, Ramirez-Meza, Castilla, Hernandez-Montes, Flores-Garza, Lopez-Saavedra, Avila-González, Martinez-Juarez, Molina-Hernández, Diaz-Martínez, Portillo and Diaz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Nestor Fabian Diaz, Instituto Nacional de Perinatología (INPER), Mexico City, 11000, México, Mexico
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