The DOI matches its Crossref record; 54 of the 56 references it cites were found in a registry or an index.
CD36, a Class B Scavenger Receptor, Is Expressed on Microglia in Alzheimer's Disease Brains and Can Mediate Production of Reactive Oxygen Species in Response to β-Amyloid Fibrils
Open accessAbstract
A pathological hallmark of Alzheimer's disease is the senile plaque, composed of beta-amyloid fibrils, microglia, astrocytes, and dystrophic neurites. We reported previously that class A scavenger receptors mediate adhesion of microglia and macrophages to beta-amyloid fibrils and oxidized low-density lipoprotein (oxLDL)-coated surfaces. We also showed that CD36, a class B scavenger receptor and an oxLDL receptor, promotes H(2)O(2) secretion by macrophages adherent to oxLDL-coated surfaces. Whether CD36 is expressed on microglia, and whether it plays a role in secretion of H(2)O(2) by microglia interacting with fibrillar beta-amyloid is not known. Using fluorescence-activated cell sorting analysis and immunohistochemistry, we found that CD36 is expressed on human fetal microglia, and N9-immortalized mouse microglia. We also found that CD36 is expressed on microglia and on vascular endothelial cells in the brains of Alzheimer's disease patients. Bowes human melanoma cells, which normally do not express CD36, gained the ability to specifically bind to surfaces coated with fibrillar beta-amyloid when transfected with a cDNA encoding human CD36, suggesting that CD36 is a receptor for fibrillar beta-amyloid. Furthermore, two different monoclonal antibodies to CD36 inhibited H(2)O(2) production by N9 microglia and human macrophages adherent to fibrillar beta-amyloid by approximately 50%. Our data identify a role for CD36 in fibrillar beta-amyloid-induced H(2)O(2) production by microglia, and imply that CD36 can mediate binding to fibrillar beta-amyloid. We propose that similar to their role in the interaction of macrophages with oxLDL, class A scavenger receptors and CD36 play complimentary roles in the interactions of microglia with fibrillar beta-amyloid.
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“Moreover, pro-oxidative events might be elicited by PCSK9 thanks to its interaction with CD36, which is expressed on microglia cells and on vascular ECs in the brain of AD patients where it promotes fibrillar Aβ-mediated H2O2 production [119].”
From The Emerging Role of PCSK9 in the Pathogenesis of Alzheimer’s Disease: A Possible Target for the Disease Treatment (2024) · cites this paper as [119]
In the citing paper
“Microglia–Aβ interactions lead to early synapse loss39, production of neurotoxic reactive oxygen and nitrogen species (ROS and RNS), NLRP3 inflammasome activation, and production of proinflammatory cytokines and TNF27,40–42.”
From Microglia in neurodegeneration (2018) · cites this paper as [40]
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“SR-B2 (also called CD36) is also a microglial Aβ receptor that forms a complex with TLR-4 and TLR-6, leading to cytokine, chemokine, and ROS production, as well as microglial migration, inflammasome activation, and neurotoxicity27,40.”
From Microglia in neurodegeneration (2018) · cites this paper as [40]
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Cites
Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red.
Lorenzo, A., & Yankner, B. A. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.25.12243 · Cited by 1,324
Activation of microglial cells by β-amyloid protein and interferon-γ
Meda, L., Cassatella, M. A., Szendrei, G. I., Otvos, L., Baron, P., Villalba, M., Ferrari, D., & Rossi, F. (1995) · Nature · doi:10.1038/374647a0 · Cited by 1,314
CD36 is a receptor for oxidized low density lipoprotein
Endemann, G., Stanton, L. W., Madden, K. S., Bryant, C. M., White, R. T., & Protter, A. A. (1993) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)50272-1 · Cited by 1,282
A role for macrophage scavenger receptors in atherosclerosis and susceptibility to infection
Suzuki, H. I., Kurihara, Y., Takeya, M., Kamada, N., Kataoka, M., Jishage, K., Ueda, O., Sakaguchi, H., Higashi, T., Suzuki, T., et al. (1997) · Nature · doi:10.1038/386292a0 · Cited by 1,226
Febbraio, M., Podrez, E. A., Smith, J. D., Hajjar, D. P., Hazen, S. L., Hoff, H. F., Sharma, K., & Silverstein, R. L. (2000) · Journal of Clinical Investigation · doi:10.1172/jci9259 · Cited by 1,037
Scavenger receptor-mediated adhesion of microglia to β-amyloid fibrils
Khoury, J. E., Hickman, S. E., Thomas, C. A., Cao, L., Silverstein, S. C., & Loike, J. D. (1996) · Nature · doi:10.1038/382716a0 · Cited by 727
Self-citationβ-Amyloid-mediated vasoactivity and vascular endothelial damage
Thomas, T., Thomas, G., McLendon, C., Sutton, T., & Mullan, M. (1996) · Nature · doi:10.1038/380168a0 · Cited by 703
Sedgwick, J. D., Schwender, S., Imrich, H., Dörries, R., Butcher, G. W., & ter Meulen, V. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.16.7438 · Cited by 691
Diversity of function is inherent in matricellular proteins: an appraisal of thrombospondin 1.
Bornstein, P. (1995) · The Journal of cell biology · doi:10.1083/jcb.130.3.503 · Cited by 666
Paresce, D. M., Ghosh, R. N., & Maxfield, F. R. (1996) · Neuron · doi:10.1016/s0896-6273(00)80187-7 · Cited by 663
Cited by
Sorted by citations
Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
Block, M. L., Zecca, L., & Hong, J.-S. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2038 · Cited by 4,110
Microglia in neurodegeneration
Hickman, S., Izzy, S., Sen, P., Morsett, L., & El Khoury, J. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0242-x · Cited by 1,710
Stewart, C. R., Stuart, L. M., Wilkinson, K., van Gils, J. M., Deng, J., Halle, A., Rayner, K. J., Boyer, L., Zhong, R., Frazier, W. A., et al. (2010) · Nature Immunology · doi:10.1038/ni.1836 · Cited by 1,513
Self-citationMicroglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice
Hickman, S. E., Allison, E. K., & El Khoury, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0616-08.2008 · Cited by 1,329
“Fluorescence intensity was measured using a FACSCalibur (BD Biosciences) flow cytometer as described previously (Coraci et al., 2002; El Khoury et al., 2007).”
CD36, a Scavenger Receptor Involved in Immunity, Metabolism, Angiogenesis, and Behavior
Silverstein, R. L., & Febbraio, M. (2009) · Science Signaling · doi:10.1126/scisignal.272re3 · Cited by 1,141
Metadata
- Authors
- Coraci, I. S., Husemann, J., Berman, J. W., Hulette, C., Dufour, J. H., Campanella, G. K., Luster, A. D., Silverstein, S. C., & El Khoury, J. B.
- Affiliations
- Columbia University Irving Medical Center (US)
- Albert Einstein College of Medicine (US)
- Duke University (US)
- Harvard University (US)
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2002-01
- Volume
- 160
- Issue
- 1
- Pages
- 101-112
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1867121
- OpenAlex
- W2096519700
- Cited by
- 398
- References
- 56
- Citations by year
- 2026: 6 · 2025: 18 · 2024: 13 · 2023: 10 · 2022: 16 · 2021: 18 · 2020: 29 · 2019: 17 · 2018: 10 · 2017: 16 · 2016: 16 · 2015: 18 · 2014: 29 · 2013: 18 · 2012: 33
- FWCI
- 7.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke
- National Heart, Lung, and Blood Institute (PO1-AG02219, P50-AG05138)
- Alzheimer's Association (R37-AI 20516)
- National Institute of Allergy and Infectious Diseases (HL43310)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- CD36, scavenger receptor class B, microglia, Alzheimer's disease, amyloid-beta fibrils, reactive oxygen species, hydrogen peroxide production, amyloid plaques, vascular endothelial cells, monoclonal antibody inhibition
- MeSH terms
- Alzheimer Disease, Animals, Antibodies, Brain, Cell Adhesion, Cell Line, Cell Line, Transformed, Fetus, Humans, Macrophages, Membrane Proteins, Peptide Fragments, Peroxides, Phagocytes, Receptors, Immunologic, Amyloid beta-Peptides, Reactive Oxygen Species, Microglia, Receptors, Lipoprotein, CD36 Antigens, Receptors, Scavenger, Scavenger Receptors, Class A, Scavenger Receptors, Class B, Mice, Rats
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