ArticlePloS one2013
Depletion of spleen macrophages delays AA amyloid development: a study performed in the rapid mouse model of AA amyloidosis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- The ASC inflammasome adapter governs SAA-derived protein aggregation in inflammatory amyloidosis.EMBO molecular medicine · 2024Article
- AA-amyloidosis in cats (Felis catus) housed in shelters.PloS one · 2023Article
- Disrupting the DREAM transcriptional repressor complex induces apolipoprotein overexpression and systemic amyloidosis in mice.The Journal of clinical investigation · 2021Article
- Tissue macrophages and interferon-gamma signalling control blood-stageCurrent research in immunology · 2021Article
- Splenomegaly in Children and Adolescents.Frontiers in pediatrics · 2021Review
- Serum Amyloid A1 Induces Classically Activated Macrophages: A Role for Enhanced Fibril Formation.Frontiers in immunology · 2021Article
- Treating Protein Misfolding Diseases: Therapeutic Successes Against Systemic Amyloidoses.Frontiers in pharmacology · 2020Review
- Apolipoprotein A-II induces acute-phase response associated AA amyloidosis in mice through conformational changes of plasma lipoprotein structure.Scientific reports · 2018Article
- Animal models of monoclonal immunoglobulin-related renal diseases.Nature reviews. Nephrology · 2018Review
- Inhibitory effect of propolis on the development of AA amyloidosis.Journal of toxicologic pathology · 2018Article
- Noncerebral Amyloidoses: Aspects on Seeding, Cross-Seeding, and Transmission.Cold Spring Harbor perspectives in medicine · 2018Review
- Post mortem findings and their relation to AA amyloidosis in free-ranging Herring gulls (Larus argentatus).PloS one · 2018Article
- Cellular mechanism of fibril formation from serum amyloid A1 protein.EMBO reports · 2017Article
- Cell-to-cell transfer of SAA1 protein in a cell culture model of systemic AA amyloidosis.Scientific reports · 2017Article
- Article
- Electron tomography reveals the fibril structure and lipid interactions in amyloid deposits.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Phagocyte depletion inhibits AA amyloid accumulation in AEF-induced huIL-6 transgenic mice.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AA amyloidosis is a systemic disease that develops secondary to chronic inflammatory diseases Macrophages are often found in the vicinity of amyloid deposits and considered to play a role in both formation and degradation of amyloid fibrils. In spleen reside at least three types of macrophages, red pulp macrophages (RPM), marginal zone macrophages (MZM), metallophilic marginal zone macrophages (MMZM). MMZM and MZM are located in the marginal zone and express a unique collection of scavenger receptors that are involved in the uptake of blood-born particles. The murine AA amyloid model that resembles the human form of the disease has been used to study amyloid effects on different macrophage populations. Amyloid was induced by intravenous injection of amyloid enhancing factor and subcutaneous injections of silver nitrate and macrophages were identified with specific antibodies. We show that MZMs are highly sensitive to amyloid and decrease in number progressively with increasing amyloid load. Total area of MMZMs is unaffected by amyloid but cells are activated and migrate into the white pulp. In a group of mice spleen macrophages were depleted by an intravenous injection of clodronate filled liposomes. Subsequent injections of AEF and silver nitrate showed a sustained amyloid development. RPMs that constitute the majority of macrophages in spleen, appear insensitive to amyloid and do not participate in amyloid formation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.