ArticlePloS one2014
Mechanisms of U87 astrocytoma cell uptake and trafficking of monomeric versus protofibril Alzheimer's disease amyloid-β proteins.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- Characterization of Cellular Alterations in a Novel NAGLU Enzyme-Deficient Cellular Model Generated from U-87MG Cell Line.Neurochemical research · 2026Article
- The role of Annexin A2 in Alzheimer's disease: From cellular functions to therapeutic potential.The FEBS journal · 2026Review
- Modeling Tay-Sachs Disease in Astrocyte-like Cells Reveals Significant Changes in the Transcriptomic Profile.International journal of molecular sciences · 2026Article
- Identification of TMED10 as A Regulator for Neuronal Exocytosis of Amyloid Beta 42.Neuroscience bulletin · 2026Article
- Amyloid-Frontiers in neuroscience · 2026Review
- Mechanistic Role of Astrocytic Rac1 Protein in Alzheimer's Disease.Aging and disease · 2025Review
- The effect of human PBMCs immobilization on their Аβ42 aggregates-dependent proinflammatory state on a cellular model of Alzheimer's disease.Frontiers in neuroscience · 2024Article
- PCSK9 Affects Astrocyte Cholesterol Metabolism and Reduces Neuron Cholesterol Supplying In Vitro: Potential Implications in Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Heparan Sulfate Proteoglycans (HSPGs) Serve as the Mediator Between Monomeric Tau and Its Subsequent Intracellular ERK1/2 Pathway Activation.Journal of molecular neuroscience : MN · 2022Article
- Amyloid Beta Is InternalizedFrontiers in molecular neuroscience · 2022Article
- Critical Molecular and Cellular Contributors to Tau Pathology.Biomedicines · 2021Review
- Deep Brain Stimulation for Alzheimer's Disease: Stimulation Parameters and Potential Mechanisms of Action.Frontiers in aging neuroscience · 2021Review
- Anodal Transcranial Direct Current Stimulation Can Improve Spatial Learning and Memory and Attenuate AβFrontiers in aging neuroscience · 2020Article
- Self-triggered click reaction in an Alzheimer's disease model:Chemical science · 2019Article
- Contribution of syndecans to cellular internalization and fibrillation of amyloid-β(1-42).Scientific reports · 2019Article
- TFEB enhances astroglial uptake of extracellular tau species and reduces tau spreading.The Journal of experimental medicine · 2018Article
- Amyloid clearance defect in ApoE4 astrocytes is reversed by epigenetic correction of endosomal pH.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Effects and mechanism of amyloid β1-42 on mitochondria in astrocytes.Molecular medicine reports · 2018Article
- Diversity of astroglial responses across human neurodegenerative disorders and brain aging.Brain pathology (Zurich, Switzerland) · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A significant hallmark of Alzheimer's disease is the formation of senile plaques in the brain due to the unbalanced levels of amyloid-beta (Aβ). However, although how Aβ is produced from amyloid precursor proteins is well understood, little is known regarding the clearance and metabolism of various Aβ aggregates from the brain. Similarly, little is known regarding how astrocytes internalize and degrade Aβ, although astrocytes are known to play an important role in plaque maintenance and Aβ clearance. The objective of this study is to investigate the cellular mechanisms that mediate the internalization of soluble monomeric versus oligomeric Aβ by astrocytes. We used a combination of laser confocal microscopy and genetic and pharmacological experiments to dissect the internalization of sAβ42 and oAβ42 and their postendocytic transport by U87 human brain astrocytoma cell line. Both Aβ42 species were internalized by U87 cells through fluid phase macropinocytosis, which required dynamin 2. Depleting LDL receptor-related protein 1 (LRP1) decreased sAβ42 uptake more significantly than that of oAβ42. We finally show that both Aβ42 species were rapidly transported to lysosomes through an endolytic pathway and subjected to proteolysis after internalization, which had no significant toxic effects to the U87 cells under relatively low concentrations. We propose that macropinocytic sAβ42 and oAβ42 uptake and their subsequent proteolytic degradation in astroglial cells is a significant mechanism underlying Aβ clearance from the extracellular milieu. Understanding the molecular events involved in astrocytic Aβ internalization may identify potential therapeutic targets for Alzheimer's disease.
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