Unaltered prion disease in mice lacking developmental endothelial locus-1.
Neurobiol Aging
; 76: 208-213, 2019 04.
Article
en En
| MEDLINE
| ID: mdl-30743056
ABSTRACT
Progression of prion diseases is driven by the accumulation of prions in the brain. Ablation of microglia or deletion of the eat-me-signal, milk-fat globule epidermal growth factor VIII (Mfge8), accelerates prion pathogenesis, suggesting that microglia defend the brain by phagocytosing prions. Similar to Mfge8, developmental endothelial locus-1 (Del-1) is a secreted protein that acts as an opsonin bridging phagocytes and apoptotic cells to facilitate phagocytosis. We therefore asked whether Del-1 might play a role in controlling prion pathogenesis. We assessed the anti-inflammatory and phagocytosis-promoting functions of Del-1 in prion disease and determined whether Del-1 complements Mfge8 in prion clearance in mice with a C57BL/6J genetic background. We found that Del-1 deficiency did not change prion disease progression or lesion patterns. In addition, prion clearance and scrapie prion protein deposition were unaltered in Del-1-deficient mice. In addition, prion-induced neuroinflammation was not affected by Del-1 deficiency. We conclude that Del-1 is not a major determinant of prion pathogenesis in this context.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Fagocitosis
/
Enfermedades por Prión
/
Eliminación de Gen
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Microglía
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Péptidos y Proteínas de Señalización Intercelular
Límite:
Animals
Idioma:
En
Revista:
Neurobiol Aging
Año:
2019
Tipo del documento:
Article
País de afiliación:
Suiza