Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/16684
Título
Low Levels of Amyloid Precursor Protein (APP) Promote Neurogenesis and Decrease Gliogenesis in Human Neural Stem Cells
Autor(es)
Coronel Lopez, Raquel ISCIII | López-Alonso, Victoria ISCIII | Gallego, Marta Ines ISCIII | Liste-Noya, Isabel ISCIII
Fecha de publicación
2023-09-27
Cita
Int J Mol Sci. 2023 Sep 27;24(19):14635.
Idioma
Inglés
Tipo de documento
research article
Resumen
Amyloid precursor protein (APP) has been widely studied due to its association with Alzheimer's disease (AD). However, the physiological functions of APP are still largely unexplored. APP is a transmembrane glycoprotein whose expression in humans is abundant in the central nervous system. Specifically, several studies have revealed the high expression of APP during brain development. Previous studies in our laboratory revealed that a transient increase in APP expression induces early cell cycle exit of human neural stem cells (hNSCs) and directs their differentiation towards glial cells (gliogenesis) while decreasing their differentiation towards neurons (neurogenesis). In the present study, we have evaluated the intrinsic cellular effects of APP down-expression (using siRNA) on cell death, cell proliferation, and cell fate specification of hNSCs. Our data indicate that APP silencing causes cellular effects opposite to those obtained in previous APP overexpression assays, inducing cell proliferation in hNS1 cells (a model line of hNSCs) and favoring neurogenesis instead of gliogenesis in these cells. In addition, we have analyzed the gene and protein expression levels of β-Catenin as a possible molecule involved in these cellular effects. These data could help to understand the biological role of APP, which is necessary to deepen the knowledge of AD.
Palabras clave
Amyloid precursor protein | Human neural stem cells | Neurogenesis | Gliogenesis | Cell fate specification | Proliferation
MESH
Alzheimer Disease | Amyloid beta-Peptides | Neurogenesis | Humans | Amyloid beta-Protein Precursor | Neural Stem Cells | Neuroglia | Neurons
Versión en línea
DOI
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