Lipid membranes accelerate amyloid formation in the mouse model of AA amyloidosis

Autor: Aida Vahdat shariat panahi, Karin Öllinger, Gunilla T. Westermark, Katarzyna Lundmark, Per Hultman
Rok vydání: 2019
Předmět:
liposomes
Amyloid
Cell- och molekylärbiologi
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology)
Molecular Biology
Microbiology
Biochemistry or Biopharmacy)
Inflammation
030204 cardiovascular system & hematology
Protein Aggregation
Pathological
Mice
03 medical and health sciences
0302 clinical medicine
AA amyloidosis
mental disorders
Internal Medicine
medicine
Animals
Serum amyloid A
Lipid bilayer
Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi)
molekylärbiologi
mikrobiologi
biokemi eller biofarmaci)
Serum Amyloid A Protein
Liposome
Chemistry
Macrophages
Acute-phase protein
Amyloidosis
medicine.disease
Lipids
macrophages
lipid membrane
Disease Models
Animal
Membrane
Biochemistry
Female
medicine.symptom
Cell and Molecular Biology
030217 neurology & neurosurgery
Zdroj: Amyloid. 26:34-44
ISSN: 1744-2818
1350-6129
DOI: 10.1080/13506129.2019.1576606
Popis: Introduction: AA amyloidosis develops as a result of prolonged inflammation and is characterized by deposits of N-terminal proteolytic fragments of the acute phase reactant serum amyloid A (SAA). Macrophages are usually found adjacent to amyloid, suggesting their involvement in the formation and/or degradation of the amyloid fibrils. Furthermore, accumulating evidence suggests that lipid membranes accelerate the fibrillation of different amyloid proteins. Methods: Using an experimental mouse model of AA amyloidosis, we compared the amyloidogenic effect of liposomes and/or amyloid-enhancing factor (AEF). Inflammation was induced by subcutaneous injection of silver nitrate followed by intravenous injection of liposomes and/or AEF to accelerate amyloid formation. Results: We showed that liposomes accelerate amyloid formation in inflamed mice, but the amyloidogenic effect of liposomes was weaker compared with AEF. Regardless of the induction method, amyloid deposits were mainly found in the marginal zones of the spleen and coincided with the depletion of marginal zone macrophages, while red pulp macrophages and metallophilic marginal zone macrophages proved insensitive to amyloid deposition. Conclusions: We conclude that increased intracellular lipid content facilitates AA amyloid fibril formation and show that the mouse model of AA amyloidosis is a suitable system for further mechanistic studies. Funding Agencies|County Council of Ostergotland; Magnus Bergvalls Research Foundation; Broderna Karlssons Research Foundation; K. Molins Minnesfond and Hildur Pettersons Research Foundation
Databáze: OpenAIRE
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