| First Author | Zhu C | Year | 2019 |
| Journal | Neurobiol Aging | Volume | 76 |
| Pages | 208-213 | PubMed ID | 30743056 |
| Mgi Jnum | J:276055 | Mgi Id | MGI:6313798 |
| Doi | 10.1016/j.neurobiolaging.2019.01.003 | Citation | Zhu C, et al. (2019) Unaltered prion disease in mice lacking developmental endothelial locus-1. Neurobiol Aging 76:208-213 |
| abstractText | 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. |
