Unaltered prion disease in mice lacking developmental endothelial locus-1
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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.
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Neither the 'eat me'-protein developmental endothelial locus-1 nor the 'don't eat me'-receptor signal regulatory protein SIRPa, nor the macrophage scavenger receptor 1 (Msr1) influence the prion disease course, since their depletion had no effect on disease pathophysiology.
“However, neither the “eat me”-protein developmental endothelial locus-1 nor the “don’t eat me”-receptor signal regulatory protein SIRPa, nor the macrophage scavenger receptor 1 (Msr1) influence the prion disease course, since their depletion had no effect on disease pathophysiology [85,86,87].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [86]
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Self-citation
- Authors
- Zhu, C., Li, Z., Li, B., Pfammatter, M., Hornemann, S., & Aguzzi, A.
- Affiliations
- University Hospital Zurich (CH)
- Corresponding author
- Aguzzi, Adriano
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 76
- Pages
- 208-213
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2950871580
- Cited by
- 4
- References
- 32
- Citations by year
- 2022: 1 · 2021: 3
- FWCI
- 0.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurobiology of Aging (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by-nc-nd)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by-nc-nd)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- European Research Council (250356)
- Swiss National Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- prion disease, developmental endothelial locus-1, Del-1, MFG-E8, phagocytosis, microglia, prion clearance, scrapie, opsonins, prion pathogenesis, C57BL/6J mice
- MeSH terms
- Animals, Calcium-Binding Proteins, Inflammation, Mice, Inbred C57BL, Mice, Transgenic, Phagocytosis, Prions, Cell Adhesion Molecules, Prion Diseases, Gene Deletion, Microglia, Intercellular Signaling Peptides and Proteins
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