CoChat
Sign Up
Cited by 116Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsInflammasome and immune disorders

Alzheimer's β-amyloid peptides induce inflammatory cascade in human vascular cells: the roles of cytokines and CD40

Suo, Zhiming, Tan, Jun, Placzek, Andon, Crawford, Fiona, Fang, Chunhong, Mullan, Michael·1998·Brain Research
DOI 10.1016/s0006-8993(98)00780-x
Open this paper in CoChat — free account

Abstract

Accumulating evidence suggests that beta-amyloid (Abeta)-induced inflammatory reactions may partially drive the pathogenesis of Alzheimer's disease (AD). Recent data also implicate similar inflammatory processes in cerebral amyloid angiopathy (CAA). To evaluate the roles of Abeta in the inflammatory processes in vascular tissues, we have tested the ability of Abeta to trigger inflammatory responses in cultured human vascular cells. We found that stimulation with Abeta dose-dependently increased the expression of CD40, and secretion of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in endothelial cells. Abeta also induced expression of IFN-gamma receptor (IFN-gammaR) both in endothelial and smooth muscle cells. Characterization of the Abeta-induced inflammatory responses in the vascular cells showed that the ligation of CD40 further increased cytokine production and/or the expression of IFN-gammaR. Moreover, IL-1beta and IFN-gamma synergistically increased the Abeta-induced expression of CD40 and IFN-gammaR. We have recently found that Abeta induces expression of adhesion molecules, and that cytokine production and interaction of CD40-CD40 ligand (CD40L) further increase the Abeta-induced expression of adhesion molecules in these same cells. These results suggest that Abeta can function as an inflammatory stimulator to activate vascular cells and induces an auto-amplified inflammatory molecular cascade, through interactions among adhesion molecules, CD40-CD40L and cytokines. Additionally, Abeta1-42, the more pathologic form of Abeta, induces much stronger effects in endothelial cells than in smooth muscle cells, while the reverse is true for Abeta1-40. Collectively, these findings support the hypothesis that the Abeta-induced inflammatory responses in vascular cells may play a significant role in the pathogenesis of CAA and AD.

Integrity signals

Registry

Crossref · 10.1016/s0006-8993(98)00780-x

Cites

42 of 42 references verified0 citation errors · 0 not checkable

Statistics

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

Claims the paper makes

We couldn’t retrieve this paper’s full text, 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?

  • In vitro treatment of endothelial cells with Aβ induced expression of IFN-γ, IL-6, IL-1β, and CD40, increasing secretion of MCP-1.

    “In vitro treatment of endothelial cells with Aβ induced expression of multiple inflammatory molecules, including IFN-γ, IL-6, IL-1β, and CD40,470,471 increasing the secretion of monocyte chemoattractant, MCP-1, which has been shown to be highly expressed in the cerebral endothelial cells from AD patients.471”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [470]

Cites

Flagged first, then by citations

1 of the 43 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Related

Authors
Suo, Z., Tan, J., Placzek, A., Crawford, F., Fang, C., & Mullan, M.
Affiliations
University of South Florida (US)
Corresponding author
Suo, Zhiming
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
1998-10
Volume
807
Issue
1-2
Pages
110-117
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/s0006-8993(98)00780-x
OpenAlex
W2052556375
Cited by
116
References
43
Citations by year
2025: 1 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 5 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 9 · 2013: 9 · 2012: 6
FWCI
3.37
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
Alzheimer's disease, amyloid-beta, cerebral amyloid angiopathy, vascular inflammation, CD40, CD40 ligand, interferon-gamma, IL-1β, interferon-gamma receptor, endothelial cells, vascular smooth muscle cells, adhesion molecules, amyloid-beta 42, Aβ40, cytokine synergy
MeSH terms
Interferon gamma Receptor, Alzheimer Disease, Cell Line, Endothelium, Vascular, Humans, Inflammation, Interferon-gamma, Interleukin-1, Muscle, Smooth, Vascular, Signal Transduction, Up-Regulation, Cytokines, Amyloid beta-Peptides, Receptors, Interferon, Intercellular Adhesion Molecule-1, CD40 Antigens, E-Selectin

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