CoChat
Sign Up
Cited by 105

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

β Amyloid peptide (Aβ 42 ) is internalized via the G‐protein‐coupled receptor FPRL1 and forms fibrillar aggregates in macrophages 1

YAZAWA, HIROSHI, YU, ZU-XI, TAKEDA, KAZUYO, LE, YINGYING, GONG, WANGHUA, FERRANS, VICTOR J., OPPENHEIM, JOOST J., LI, CHOU CHI H., WANG, JI MING·2001·The FASEB Journal
DOI 10.1096/fj.01-0251com
Open this paper in CoChat — free account

Abstract

The 42 amino acid form of β amyloid (Aβ 42 ) plays a pivotal role in neurotoxicity and the activation of mononuclear phagocytes in Alzheimer's disease (AD). Our recent study revealed that FPRL1, a G‐protein‐coupled receptor, mediates the chemotactic and activating effect of Aβ 42 on mononuclear phagocytes (monocytes and microglia), suggesting that FPRL1 may be involved in the proinflammatory responses in AD. We investigated the role of FPRL1 in cellular uptake and the subsequent fibrillar formation of Aβ 42 by using fluorescence confocal microscopy. We found that upon incubation with macrophages or HEK293 cells genetically engineered to express FPRL1, Aβ 42 associated with FPRL1 and the Aβ 42 /FPRL1 complexes were rapidly internalized into the cytoplasmic compartment. The maximal internalization of Aβ 42 / FPRL1 complexes occurred by 30 min after incubation. Removal of free Aβ 42 from culture supernatants at 30 min resulted in a progressive recycling of FPRL1 to the cell surface and degradation of the internalized Aβ 42 . However, persistent exposure of the cells to Aβ 42 over 24 h resulted in retention of Aβ 42 /FPRL1 complexes in the cytoplasmic compartment and the formation of Congo red positive fibrils in macrophages but not in HEK 293 cell transfected with FPRL 1. These results suggest that besides mediating the proinflammatory activity of Aβ 42 , FPRL1 is also involved in the internalization of Aβ 42 , which culminates in the formation of fibrils only in macrophages.—Yazawa, H., Yu, Z.‐X., Takeda, K., Le, Y., Gong, W., Ferrans, V. J., Oppenheim, J. J., Li, C. C. H., Wang, J. M. β Amyloid peptide (Aβ 42 ) is internalized via the G‐protein‐coupled receptor FPRL1 and forms fibrillar aggregates in macrophages. FASEB J. 15 , 2454–2462 (2001)

Overview

Integrity signals

Registry

Crossref · 10.1096/fj.01-0251com

Cites

11 of 11 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 47

  1. 10.1038/399a023 · DOI · Paper page
  2. 10.1523/JNEUROSCI.19-20-08876.1999 · DOI · Paper page
  3. 10.1073/pnas.91.25.12243 · DOI · Paper page
  4. 10.1016/S0166-2236(00)01749-5 · DOI · Paper page
  5. 10.1038/sj.mp.4000212 · DOI
  6. 10.1002/jlb.65.4.409 · DOI
  7. 10.1097/00062752-199901000-00004 · DOI
  8. 10.1073/pnas.93.9.4147 · DOI
  9. 10.1002/glia.440070105 · DOI
  10. 10.1016/0014-5793(87)80305-8 · DOI
  11. 10.4049/jimmunol.149.8.2736 · DOI
  12. 10.1016/S0165-5728(96)00110-5 · DOI
  13. 10.1212/WNL.47.2.425 · DOI · Paper page
  14. 10.1016/S1359-6446(99)01339-2 · DOI
  15. El Khoury J., 1998, Microglia, scavenger receptors, and the pathogenesis of Alzheimer's disease, Neurobiol. Aging, 19, S81, 10.1016/S0197-4580(98)00036-0 · DOI
  16. 10.1016/S0896-6273(00)80187-7 · DOI · Paper page
  17. 10.1006/exnr.1999.7265 · DOI
  18. 10.1523/JNEUROSCI.18-12-04451.1998 · DOI
  19. 10.1016/S0197-4580(00)00092-0 · DOI
  20. 10.1523/JNEUROSCI.19-03-00928.1999 · DOI
  21. 10.1523/JNEUROSCI.21-02-j0003.2001 · DOI
  22. 10.1074/jbc.M101031200 · DOI
  23. Le Y., 1999, Utilization of two seven-trans-membrane, G protein-coupled receptors, formyl peptide receptor-like 1 and formyl peptide receptor, by the synthetic hexapep-tide WKYMVm for human phagocyte activation, J. Immunol., 163, 6777, 10.4049/jimmunol.163.12.6777 · DOI
  24. 10.1182/blood.V84.5.1415.1415 · DOI
  25. 10.1084/jem.182.5.1545 · DOI · Paper page
  26. Heidenreich S., 1997, Regulation of human monocyte apoptosis by the CD14 molecule, J. Immunol., 159, 3178, 10.4049/jimmunol.159.7.3178 · DOI
  27. Mangan D. F., 1991, Lipopoly-saccharide, tumor necrosis factor-alpha, and IL-1 beta prevent programmed cell death (apoptosis) in human peripheral blood monocytes, J. Immunol., 146, 1541, 10.4049/jimmunol.146.5.1541 · DOI
  28. Seo J. K., 1998, Distribution of the receptor for a novel peptide stimulating phosphoinosi-tide hydrolysis in human leukocytes, Clin. Biochem., 31, 137, 10.1016/S0009-9120(97)00172-0 · DOI
  29. 10.1006/bbrc.1999.0552 · DOI
  30. 10.1002/1531-8249(199912)46:6<860::AID-ANA8>3.0.CO;2-M · DOI
  31. Funato H., 1998, Quantitation of amyloid beta-protein (A beta) in the cortex during aging and in Alzheimer's disease, Am. J. Pathol., 152, 1633
  32. Rossi M., 1996, Structural analysis of the substoichiometric and stoichiometric microtubule-inhibiting bi-phenyl analogues of colchicine, Biochemistry, 35, 3286, 10.1021/bi950524p · DOI
  33. 10.1016/S0165-5728(97)00128-8 · DOI
  34. Heinzelmann M., 1999, Endocytosis of heparin-binding protein (CAP37) is essential for the enhancement of lipopolysaccharide-induced TNF-alpha production in human monocytes, J. Immunol., 162, 4240, 10.4049/jimmunol.162.7.4240 · DOI
  35. 10.1084/jem.184.5.1737 · DOI
  36. 10.1016/S0165-5728(98)00188-X · DOI
  37. Breitner J. C., 1995, Onset of Alzheimer's disease with nonsteroidal anti-inflammatory and histamine H2 blocking drugs, Aging, 16, 523
  38. Zastrow M., 1992, Ligand-regulated internalization and recycling of human beta 2-adrenergic receptors between the plasma membrane and endosomes containing transferrin receptors, J. Biol. Chem., 267, 3530, 10.1016/S0021-9258(19)50762-1 · DOI
  39. 10.1016/S0021-9258(18)86921-6 · DOI
  40. 10.1074/jbc.271.31.18302 · DOI
  41. 10.1016/S0163-7258(96)00203-3 · DOI
  42. 10.1074/jbc.C000314200 · DOI
  43. 10.1016/0197-4580(95)00092-S · DOI · Paper page
  44. 10.1046/j.1471-4159.1999.0720443.x · DOI
  45. 10.1016/0197-4580(95)00055-J · DOI
  46. 10.1074/jbc.274.45.32301 · DOI · Paper page
  47. 10.1002/(SICI)1097-4547(20000215)59:4<522::AID-JNR7>3.0.CO;2-L · DOI

Cited by

Sorted by citations

Metadata

Authors
YAZAWA, H., YU, Z.-X., TAKEDA, K., LE, Y., GONG, W., FERRANS, V. J., OPPENHEIM, J. J., LI, C. C. H., & WANG, J. M.
Affiliations
  • Laboratory of Molecular Immunoregulation National Cancer Institute at Frederick Frederick Maryland 21702 USA
  • Pathology Section, National Heart, Lung, and Blood Institute National Institutes of Health Bethesda Maryland 20892 USA
  • Intramural Research Support Program SAIC Frederick Center for Cancer Research National Cancer Institute at Frederick Frederick Maryland 21702 USA
Venue
The FASEB Journal
Publisher
Wiley
Published
2001-11
Volume
15
Issue
13
Pages
2454-2462
ISSN
  • 0892-6638
  • 1530-6860
DOI
10.1096/fj.01-0251com
Cited by
105
References
11
Language
en
Licence

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review