Unaltered prion disease in mice lacking developmental endothelial locus-1

NEUROBIOLOGY OF AGING

卷:76

Article

Zhu, Caihong¹  Li, Zhihao¹  Li, Bei¹  Pfammatter, Manuela¹  Hornemann, Simone¹  Aguzzi, Adriano¹ 

[1] Univ Hosp Zurich, Inst Neuropathol, Schmelzbergstr 12, CH-8091 Zurich, Switzerland

关键词: Prion disease;    Del-1;    Phagocytosis;    Microglial activation;    Neuroinflammation;   

DOI  :  10.1016/j.neurobiolaging.2019.01.003

来源: Elsevier

【 摘 要 】

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. (C) 2019 Elsevier Inc. All rights reserved.

【 授权许可】

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