Related Experiment Video
Updated: Jan 29, 2026
Real-time Quaking-induced Conversion Assay for Detection of CWD Prions in Fecal Material
Published on: September 29, 2017
Unaltered prion disease in mice lacking developmental endothelial locus-1
Caihong Zhu1, Zhihao Li1, Bei Li1
1Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland.
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.
Insights
Developmental endothelial locus-1 (Del-1) does not influence prion disease progression or neuroinflammation. This study found Del-1 deficiency did not alter prion clearance or scrapie prion protein deposition in mice.
Area of Science:
- Neuroscience
- Immunology
- Prion Biology
Background:
- Prion diseases are characterized by prion accumulation in the brain.
- Microglia phagocytosis of prions is a key defense mechanism.
- Milk-fat globule epidermal growth factor VIII (Mfge8) facilitates microglial phagocytosis.
Purpose of the Study:
- To investigate the role of developmental endothelial locus-1 (Del-1) in prion disease pathogenesis.
- To assess Del-1's function in prion clearance and neuroinflammation.
- To determine if Del-1 complements Mfge8 in controlling prion accumulation.
Main Methods:
- Assessed prion disease progression and lesion patterns in Del-1 deficient mice.
- Measured prion clearance and scrapie prion protein deposition.
- Evaluated prion-induced neuroinflammation in the absence of Del-1.
Main Results:
- Del-1 deficiency did not alter prion disease progression or lesion patterns.
- Prion clearance and scrapie prion protein deposition remained unchanged in Del-1 deficient mice.
- Prion-induced neuroinflammation was not affected by Del-1 deficiency.
Conclusions:
- Developmental endothelial locus-1 (Del-1) does not appear to be a major determinant of prion pathogenesis.
- Del-1 does not play a significant role in prion clearance or modulating neuroinflammation in this model.
- The function of Del-1 in phagocytosis does not significantly impact prion disease control.
Related Concept Videos
01:26Locus of Control
01:19Root-Locus Method
This system can be represented by a block...
01:15Construction of Root Locus
For positive gain values, the root locus exists on the real axis to the left of an odd number of finite open-loop poles or zeros. The root locus starts at the open-loop poles and traces the paths of the closed-loop poles as the gain...
01:05Properties of the Root Locus
To determine if a point lies on the root locus, the criterion involves the sum of angles contributed by all poles and zeros to that point. Specifically, this sum must be an odd multiple of 180 degrees. The gain at any point on...
01:14Rotter's Locus of Control
Individuals with an internal locus of control believe that their personal efforts and decisions directly affect their...
01:27Introduction to Developmental Psychology