Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Más filtros











Base de datos
Tipo de estudio
Intervalo de año de publicación
1.
In Vitro Cell Dev Biol Anim ; 57(4): 415-427, 2021 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-33748906

RESUMEN

Although originally discovered inducing important biological functions in the nervous system, repulsive guidance molecule a (RGMa) has now been identified as a player in many other processes and diseases, including in myogenesis. RGMa is known to be expressed in skeletal muscle cells, from somites to the adult. Functional in vitro studies have revealed that RGMa overexpression could promote skeletal muscle cell hypertrophy and hyperplasia, as higher efficiency in cell fusion was observed. Here, we extend the potential role of RGMa during C2C12 cell differentiation in vitro. Our results showed that RGMa administrated as a recombinant protein during late stages of C2C12 myogenic differentiation could induce myoblast cell fusion and the downregulation of different myogenic markers, while its administration at early stages induced the expression of myogenic markers with no detectable morphological effects. We also found that RGMa effects on skeletal muscle hyperplasia are performed via neogenin receptor, possibly as part of a complex with other proteins. Additionally, we observed that RGMa-neogenin is not playing a role as an inhibitor of the BMP signalling in skeletal muscle cells. This work contributes to placing RGMa as a component of the mechanisms that determine skeletal cell fusion via neogenin receptor.


Asunto(s)
Diferenciación Celular/genética , Proteínas Ligadas a GPI/genética , Hiperplasia/genética , Proteínas de la Membrana/genética , Proteínas del Tejido Nervioso/genética , Animales , Línea Celular , Regulación del Desarrollo de la Expresión Génica/genética , Humanos , Hiperplasia/patología , Ratones , Desarrollo de Músculos/genética , Fibras Musculares Esqueléticas/metabolismo , Fibras Musculares Esqueléticas/patología , Transducción de Señal/genética
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA