Amyloid-β-Induced Astrocytic Phagocytosis is Mediated by CD36, CD47 and RAGE
Abstract
Astrocytes, the most numerous glial cell in the brain, have multiple functions and are key to maintenance of homeostasis in the central nervous system. Microglia are the resident immunocompetent cells in the brain and share several functions with macrophages, including their phagocytic ability. Indeed microglia are the resident phagocytes in the brain and express numerous cell surface proteins which act to enable receptor-mediated phagocytosis. However recent evidence suggests that astrocytes express some genes which permit phagocytosis of phosphatidylserine-decorated cells and this probably explains sporadic reports in the literature which suggest that astrocytes become phagocytic following brain trauma. Here we examined the potential of astrocytes to phagocytose fluorescently-labelled latex beads and amyloid-β (Aβ) and report that they competently engulf both in a manner that relies on actin polymerization since it was inhibited by cytochalasin D. The data indicate that incubation of cultured astrocytes or microglia with Aβ increased phagocytosis and markers of activation of both cell types. Aβ was found to markedly increase expression of the putative Aβ-binding receptors CD36 and CD47 in astrocytes, while it decreased expression of the receptor for advanced glycation endproducts (RAGE). It is demonstrated that blocking these receptors using a neutralizing antibody attenuated Aβ-induced phagocytosis of latex beads by astrocytes. Interestingly blocking these receptors also decreased uptake of beads even in the absence of Aβ. Here we demonstrate that astrocytes are competent phagocytes and are capable of engulfing Aβ.
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Blocking CD36, CD47, and RAGE with neutralizing antibodies attenuates astrocytic phagocytosis of Aβ, implicating these as putative Aβ receptors in astrocytes.
“Blocking receptors including CD36, CD47, and RAGE with neutralizing antibodies can attenuate astrocytic phagocytosis of Aβ, implicating they are putative Aβ receptors in astrocytes [407].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [407]
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“Fatty acid translocase (FAT/CD36) FAT Increased expression upon treatment with amyloid-β [50].”
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“…soluble and insoluble Ab (Wisniewski and Wegiel, 1991; Funato et al., 1998; Wyss-Coray et al., 2003; Nielsen et al., 2009; Chung et al., 2013; Jones et al., 2013; R. X. Liu et al., 2016) and degrade them via the late endolysosomal pathway (Shaffer et al., 1995; Wyss-Coray et al., 2003;…”
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T Cells—Protective or Pathogenic in Alzheimer’s Disease?
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“…that these cells express TLRs and pattern recognition receptors (PRRs) (Bowman et al. 2003; Jack et al. 2005), are capable of phagocytosis, including phagocytosis of Aβ (Jones et al. 2013) and can produce pro-inflammatory cytokines upon activation (Chastain et al. 2011; Dong and Benveniste 2001).”
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“Lyophilized Aβ1−42 peptide (SIGMA, A9810) and reverse peptide Aβ42−1 (SIGMA, SCP0048) were diluted to 1mg/ml using sterile PBS and incubated at 37◦C, 220 rpm for 48 h allowed to aggregate as described (Jones et al., 2013).”
MethodActivated Scavenger Receptor A Promotes Glial Internalization of Aβ
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“Aside from microglia, astrocytes are also considered main phagocytes that can engulf Ab [20].”
BackgroundPotential neurotoxic activity of diverse molecules released by astrocytes
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“In addition, individual neutralization of CD36, CD47, or RAGE in astrocytes partially inhibits their phagocytic capability (Jones et al., 2013).”
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Monitoring phagocytic uptake of amyloid β into glial cell lysosomes in real time
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Heme and hemoglobin suppress amyloid β–mediated inflammatory activation of mouse astrocytes
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“Aβ is highly promiscuous (47) although key astrocyte scavenger receptors include CD36, RAGE, and CD47 (48).”
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“Additionally, astrocytes have demonstrated a RAGE-mediated phagocytic ability to engulf Aβ [102].”
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“tein E (ApoE), CD36, CD47, advanced glycation end products receptor (RAGE), neprilysin (NEP), angiotensin-converting enzyme-1 (ACE-1), and endothelin-converting enzyme-2 (ECE-2) [16,19,22–26].”
BackgroundPhagocytic Glial Cells in Brain Homeostasis
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CD47 in the Brain and Neurodegeneration: An Update on the Role in Neuroinflammatory Pathways
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“During neurological disorders, CD47 functions as a key neuroimmune modulator responding to chronic and acute CNS injuries and in the process of recovery [5,8].”
BackgroundLinking T cells to Alzheimer's disease: from neurodegeneration to neurorepair
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“Ab also impacts on glial function; it activates both microglia and astrocytes in vitro triggering production and release of proinflammatory cytokines [3], and reactive oxygen and nitrogen species, all of which can have a detrimental effect on neuronal function [4].”
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“In the early phases of AD, microglia activated by A β attempt to eliminate A β deposits by inducing CD36 expression and stimulating phagocytosis in astrocytes and microglia [103,107,108].”
An Overview of Astrocyte Responses in Genetically Induced Alzheimer’s Disease Mouse Models
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Astrocytes: From the Physiology to the Disease
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The Role of Glial Mitochondria in α-Synuclein Toxicity
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“Accumulating evidence suggests that the loss of proper phagocytic functions in astrocytes may contribute to neurodegenerative processes (Jones et al., 2013; Tong et al., 2014; Chung et al., 2016).”
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Inhibition of JAK2 attenuates the increase in inflammatory markers in microglia from APP/PS1 mice
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“Primary microglia were prepared from brains of 1-day-old neonatal mice (Bioresources Unit, Trinity College, Dublin, Ireland) as described previously (Jones et al., 2013).”
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“[81] R.”
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“Another hypothesis that could be deduced from our data will attribute participation of CD36 in forming clusters of various pattern recognition receptors, including RAGE and/or Toll-like receptors (Drage et al. 2009; Jimenez-Dalmaroni et al. 2009; Xanthis et al. 2009; Jones et al. 2013).”
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“Furthermore, blocking these receptors significantly reduces the phagocytic capacity of astrocytes [93].”
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“Several candidate molecules for Aβ uptake were reported; LRP, receptor of advanced glycation end product (RAGE), CD36 and CD47 [59].”
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“We detected significant transcriptional enrichment of phagocytosis-associated TAM family members Tyro3 and Axl , complement factor C4b , and the scavenger receptor Cd36 in our within-retina comparison (Jones et al., 2013; Konishi et al., 2022).”
- Authors
- Jones, R. S., Minogue, A. M., Connor, T. J., & Lynch, M. A.
- Affiliations
- Trinity College Dublin (IE)
- Corresponding author
- Minogue, Aedín M.
- ORCID
- Lynch, Marina A.
- Venue
- Journal of Neuroimmune Pharmacology
- Published
- 2012-12-14
- Volume
- 8
- Issue
- 1
- Pages
- 301-311
- ISSN
- 1557-1890 (ISSN-L)
- 1557-1904
- OpenAlex
- W2036955747
- Cited by
- 147
- References
- 46
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 10 · 2023: 9 · 2022: 13 · 2021: 19 · 2020: 17 · 2019: 6 · 2018: 7 · 2017: 15 · 2016: 12 · 2015: 7 · 2014: 15 · 2013: 2
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neuroimmune Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Health Research Board
- Science Foundation Ireland
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- amyloid-beta, astrocytes, phagocytosis, CD36, CD47, RAGE, actin polymerization, microglia, receptor-mediated phagocytosis, receptor antagonists, neuroinflammation
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Animals, Newborn, Astrocytes, Cell Survival, Flow Cytometry, Fluorescent Dyes, Glial Fibrillary Acidic Protein, L-Lactate Dehydrogenase, Microspheres, Phagocytosis, Receptors, Immunologic, RNA, Messenger, Amyloid beta-Peptides, Fluorescein-5-isothiocyanate, Rats, Wistar, Microglia, CD36 Antigens, Excitatory Amino Acid Transporter 2, CD11b Antigen, Rats, CD47 Antigen
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