ArticleThe Journal of biological chemistry2015
Cellular interaction and cytotoxicity of the iowa mutation of apolipoprotein A-I (ApoA-IIowa) amyloid mediated by sulfate moieties of heparan sulfate.
Article in The Journal of biological chemistry, 2015. 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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17 citing papers in PubMed, 31 citations in OpenAlex.
- Multi-omic analysis of meningeal cerebral amyloid angiopathy reveals enrichment of unsubstituted glucosamine and extracellular proteins.Journal of neuropathology and experimental neurology · 2025Article
- Vascular Heparan Sulfate and Amyloid-β in Alzheimer's Disease Patients.International journal of molecular sciences · 2024Article
- Heparan sulfate proteoglycan in Alzheimer's disease: aberrant expression and functions in molecular pathways related to amyloid-β metabolism.American journal of physiology. Cell physiology · 2023Review
- The Apparent Organ-Specificity of Amyloidogenic ApoA-I Variants Is Linked to Tissue-Specific Extracellular Matrix Components.International journal of molecular sciences · 2022Article
- Design and Synthesis of 6-O-Phosphorylated Heparan Sulfate Oligosaccharides to Inhibit Amyloid β Aggregation.Chembiochem : a European journal of chemical biology · 2022Article
- Autophagy Alteration in ApoA-I Related Systemic Amyloidosis.International journal of molecular sciences · 2022Article
- A crosslinked dextran sulfate-chitosan nanoparticle for delivery of therapeutic heparin-binding proteins.International journal of pharmaceutics · 2021Article
- Apolipoprotein A1, the neglected relative of Apolipoprotein E and its potential role in Alzheimer's disease.Neural regeneration research · 2021Review
- Cell-to-cell transmission of p53 aggregates: a novel player in oncology?Molecular & cellular oncology · 2021Article
- Sulfated glycosaminoglycans mediate prion-like behavior of p53 aggregates.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Heparan sulfate S-domains and extracellular sulfatases (Sulfs): their possible roles in protein aggregation diseases.Glycoconjugate journal · 2018Review
- Effect of Phosphatidylserine and Cholesterol on Membrane-mediated Fibril Formation by the N-terminal Amyloidogenic Fragment of Apolipoprotein A-I.Scientific reports · 2018Article
- Toxic HypF-N Oligomers Selectively Bind the Plasma Membrane to Impair Cell Adhesion Capability.Biophysical journal · 2018Article
- Sulfated glycosaminoglycans in protein aggregation diseases.Glycoconjugate journal · 2017Review
- Immunochemical Approach for Monitoring of Structural Transition of ApoA-I upon HDL Formation Using Novel Monoclonal Antibodies.Scientific reports · 2017Article
- Iowa Mutant Apolipoprotein A-I (ApoA-IIowa) Fibrils Target Lysosomes.Scientific reports · 2016Article
- Enzymatic remodeling of heparan sulfate: a therapeutic strategy for systemic and localized amyloidoses?Neural regeneration research · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The single amino acid mutation G26R in human apolipoprotein A-I (apoA-I) is associated with familial amyloid polyneuropathy III. ApoA-I carrying this mutation (apoA-IIowa) forms amyloid fibrils in vitro. Heparan sulfate (HS) is a glycosaminoglycan that is abundant at the cell surface and in the extracellular matrix. Although HS and its highly sulfated domains are involved in aggregation of amyloid-β and accumulate in cerebral amyloid plaques of patients with Alzheimer disease and mouse models of this disease, the role of HS in familial amyloid polyneuropathy III has never been addressed. Here, we used cell models to investigate the possible role of HS in the cytotoxicity of apoA-IIowa amyloid. Wild-type CHO cells, but not pgsD-677 cells, an HS-deficient CHO mutant, demonstrated uptake of apoA-IIowa amyloid after incubation with the amyloid. Addition of sulfated glycosaminoglycans to culture media prevented interaction with and cytotoxicity of apoA-IIowa amyloid to CHO cells. Elimination of cell surface HS or inhibition of HS sulfation with chemical reagents interfered with interaction of apoA-IIowa amyloid with CHO cells. We also found that cellular interaction and cytotoxicity of apoA-IIowa amyloid were significantly attenuated in CHO cells that stably expressed the human extracellular endoglucosamine 6-sulfatases HSulf-1 and HSulf-2. Our results thus suggest that cell surface HS mediates cytotoxicity of apoA-IIowa amyloid and that enzymatic remodeling of HS mitigates the cytotoxicity.
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