ArticleJournal of lipid research2011
ApoA-I deficiency in mice is associated with redistribution of apoA-II and aggravated AApoAII amyloidosis.
Article in Journal of lipid research, 2011. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Proteomic and Lipidomic Atlas of Gut-Associated Lymph and Venous Depots in Female Piglets.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Exchangeable APOA1 on HDL inhibits LDL binding to proteoglycans.Journal of lipid research · 2025Article
- Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025Review
- The Role of APOA-I in Alzheimer's Disease: Bridging Peripheral Tissues and the Central Nervous System.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Temporal Profiling of Cellular and Molecular Processes in Osteodifferentiation of Dental Pulp Stem Cells.Biology · 2025Article
- Apolipoprotein A-II, a Player in Multiple Processes and Diseases.Biomedicines · 2022Review
- Disrupting the DREAM transcriptional repressor complex induces apolipoprotein overexpression and systemic amyloidosis in mice.The Journal of clinical investigation · 2021Article
- Suppression of Mouse AApoAII Amyloidosis Progression by Daily Supplementation with Oxidative Stress Inhibitors.Oxidative medicine and cellular longevity · 2019Article
- Accelerated pre-senile systemic amyloidosis in PACAP knockout mice - a protective role of PACAP in age-related degenerative processes.The Journal of pathology · 2018Article
- Apolipoprotein A-II induces acute-phase response associated AA amyloidosis in mice through conformational changes of plasma lipoprotein structure.Scientific reports · 2018Article
- Article
- Apolipoprotein A-1 regulates osteoblast and lipoblast precursor cells in mice.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Cholesterol-Independent Suppression of Lymphocyte Activation, Autoimmunity, and Glomerulonephritis by Apolipoprotein A-I in Normocholesterolemic Lupus-Prone Mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- C-terminal sequence of amyloid-resistant type F apolipoprotein A-II inhibits amyloid fibril formation of apolipoprotein A-II in mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Alginic acid cell entrapment: a novel method for measuring in vivo macrophage cholesterol homeostasis.Journal of lipid research · 2015Article
- Article
- High yield expression and purification of recombinant human apolipoprotein A-II in Escherichia coli.Journal of lipid research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein A-II (apoA-II) is the second major apolipoprotein following apolipoprotein A-I (apoA-I) in HDL. ApoA-II has multiple physiological functions and can form senile amyloid fibrils (AApoAII) in mice. Most circulating apoA-II is present in lipoprotein A-I/A-II. To study the influence of apoA-I on apoA-II and AApoAII amyloidosis, apoA-I-deficient (C57BL/6J.Apoa1⁻/⁻) mice were used. Apoa1⁻/⁻ mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels. Unexpectedly, we found that apoA-I deficiency led to redistribution of apoA-II in HDL and an age-related increase in apoA-II levels, accompanied by larger HDL particle size and an age-related increase in TC, HDL-C, and TG. Aggravated AApoAII amyloidosis was induced in Apoa1⁻/⁻ mice systemically, especially in the heart. These results indicate that apoA-I plays key roles in maintaining apoA-II distribution and HDL particle size. Furthermore, apoA-II redistribution may be the main reason for aggravated AApoAII amyloidosis in Apoa1⁻/⁻ mice. These results may shed new light on the relationship between apoA-I and apoA-II as well as provide new information concerning amyloidosis mechanism and therapy.
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Registered trials
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.