The cellular prion protein promotes neuronal regeneration after acute nasotoxic injury
| Autor: | Julie A. Moreno, Stephanie S Suinn, Glenn C. Telling, Jenna Crowell, Richard A. Bessen, Lindsay E. Parrie |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male Cell type Cell Survival animal diseases proliferation Neurogenesis Cellular prion Sensory system Mice Transgenic Biology Biochemistry Olfactory Receptor Neurons Prion Proteins 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Olfactory Mucosa medicine Animals Prion protein Axon Cell Proliferation Methimazole Mechanism (biology) Cell growth Regeneration (biology) Cell Differentiation Cell Biology differentiation Axons Cell biology nervous system diseases Nerve Regeneration 030104 developmental biology Infectious Diseases medicine.anatomical_structure regeneration neurotoxic injury Acute Disease Female 030217 neurology & neurosurgery Research Paper |
| Zdroj: | Prion |
| ISSN: | 1933-690X 1933-6896 |
| Popis: | Adult neurogenesis, analogous to early development, is comprised of several, often concomitant, processes including proliferation, differentiation, and formation of synaptic connections. However, due to continual, asynchronous turn-over, newly-born adult olfactory sensory neurons (OSNs) must integrate into existing circuitry. Additionally, OSNs express high levels of cellular prion protein (PrPC), particularly in the axon, which implies a role in this cell type. The cellular prion has been shown to be important for proper adult OSN neurogenesis primarily by stabilizing mature olfactory neurons within this circuitry. However, the role of PrPC on each specific adult neurogenic processes remains to be investigated in detail. To tease out the subtle effects of prion protein expression level, a large population of regenerating neurons must be investigated. The thyroid drug methimazole (MTZ) causes nearly complete OSN loss in rodents and is used as a model of acute olfactory injury, providing a mechanism to induce synchronized OSN regeneration. This study investigated the effect of PrPC on adult neurogenesis after acute nasotoxic injury. Altered PrPC levels affected olfactory sensory epithelial (OSE) regeneration, cell proliferation, and differentiation. Attempts to investigate the role of PrPC level on axon regeneration did not support previous studies, and glomerular targeting did not recover to vehicle-treated levels, even by 20 weeks. Together, these studies demonstrate that the cellular prion protein is critical for regeneration of neurons, whereby increased PrPC levels promote early neurogenesis, and that lack of PrPC delays the regeneration of this tissue after acute injury. |
| Databáze: | OpenAIRE |
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