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

The DOI matches its Crossref record; 42 of the 43 references it cites were found in a registry or an index.

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
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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.

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  1. M. Tewari, V.M. Dixit, Signalling through members of the tumor necrosis factor receptor family, in: C.H. Heldin, M. Purton (Eds.), Signal Transduction, Chapman & Hall, London, 1996, pp. 79–92.

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Metadata

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
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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

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