Analysis of early transcriptional changes in response to spinal cord damage in Xenopus laevis.
Unlike mammals, Xenopus laevis larvae can recover anatomically and functionally after spinal cord injury. The ependymal zone of the central canal of the spinal cord of these animals has a high percentage of Sox2+ neuronal progenitor cells. These are activated rapidly in response to injury and are ne...
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| Tipo de recurso: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2019 |
| País: | Chile |
| OAI Identifier: | oai:repositorio.anid.cl:10533/246324 |
| Acceso en línea: | https://hdl.handle.net/10533/246324 |
| Access Level: | acceso abierto |
| Palabra clave: | Ciencias Naturales Otras Ciencias Naturales |
| Sumario: | Unlike mammals, Xenopus laevis larvae can recover anatomically and functionally after spinal cord injury. The ependymal zone of the central canal of the spinal cord of these animals has a high percentage of Sox2+ neuronal progenitor cells. These are activated rapidly in response to injury and are necessary for spinal cord regeneration. Our interest is to identify the genetic network and signaling pathways involved in the early activation of this cell population. Analysis of the early transcriptional changes after injury, allowed us to propose a model of Sox2+ cells activation, which identifies new molecular components that could be key during this process, in which the mTORC1 signaling pathway would play a central role. The first validations of this model confirmed a rapid activation of the mTORC1 pathway at 3 hours after a transection, mainly in the cells of the ependymal area of the central canal near the lesion and in neuronal bodies throughout the nervous system. On the other hand, the inhibition of mTORC1 using rapamycin blocked the proliferation of Sox2+ cells and functional recovery after transection. These results suggest a key role for the mTORC1 pathway in the rapid activation of Sox2+ cells, partially validating our model and thus suggesting a series of new targets that could be key in our quest to improve the regenerative capacity of mammals. |
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