Pro-inflammatory effect of freshly solubilized β-amyloid peptides in the brain
Abstract
It has recently been shown that the level of soluble beta-amyloid (Abeta) peptides correlates well with the severity of synaptic loss and the density of neurofibrillary tangles observed in Alzheimer's disease (AD) brain. However, the biological activity of soluble forms of Abeta peptides in the brain remains to be determined. We have investigated ex vivo the effect of freshly solubilized Abeta1-40 peptides (fsAbeta) on prostaglandin E2 (PGE2) production in rat brain slices. PGE2 levels increased rapidly following treatment with fsAbeta, an effect that was prevented by SB202190, a selective inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and by NS-398, which preferentially inhibits cyclooxygenase-2 (COX-2) compared to COX-1. In an attempt to determine the cellular systems of the brain responsible for prostaglandin production in response to fsAbeta, the effect of fsAbeta was tested on isolated brain microvessels, primary cultures of brain smooth muscle cells/pericytes and endothelial cells, and a human neuron-like cell line (IMR32). Our data show that fsAbeta ex vivo can stimulate prostaglandin accumulation in incubates of isolated rat brain microvessels. In addition, fsAbeta appears to cause a concentration-dependent enhancement of prostaglandin accumulation in primary cultures of brain microvessel-derived smooth muscle cells/pericytes but not of brain endothelial cells. Finally, fsAbeta also stimulated PGF2alpha accumulation in cultures of differentiated IMR32 cells, but to a lesser extent than in brain smooth muscle cell/pericyte cultures. Deposition of aggregated forms of Abeta in the brain has been thought to trigger an inflammatory response which accompanies the neuropathologic events of AD. Our data provide evidence that fsAbeta triggers a pro-inflammatory reaction in rat brain, and suggest that the cerebrovasculature may constitute an important source of pro-inflammatory eicosanoids.
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Pericytes are an important source of pro-inflammatory eicosanoids after activation by Aβ.
“In addition, pericytes are also suggested to be an important source of pro-inflammatory eicosanoids after being activated by Aβ.500”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [500]
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- Authors
- Paris, D., Townsend, K. P., Obregon, D. F., Humphrey, J., & Mullan, M.
- Affiliations
- University of South Florida (US)
- Corresponding author
- Paris, Daniel
- Venue
- Prostaglandins & Other Lipid Mediators
- Publisher
- Elsevier BV
- Published
- 2002-09
- Volume
- 70
- Issue
- 1-2
- Pages
- 1-12
- ISSN
- 1098-8823 (ISSN-L)
- OpenAlex
- W1992280830
- Cited by
- 40
- References
- 42
- Citations by year
- 2024: 1 · 2023: 2 · 2022: 1 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 1 · 2014: 1 · 2012: 5
- FWCI
- 1.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Prostaglandins & Other Lipid Mediators (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG019250, AG19250-01)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- Aβ40, Alzheimer's disease, pro-inflammatory effects, prostaglandin E2, prostaglandin F2alpha, p38 MAPK, cyclooxygenase-2, cerebral microvasculature, pericytes, smooth muscle cells, endothelial cells, cerebrovascular inflammation, eicosanoids, neuroinflammation
- MeSH terms
- Alzheimer Disease, Animals, Brain, Cattle, Cells, Cultured, Humans, Inflammation, Isoenzymes, Male, Membrane Proteins, Nitrobenzenes, Prostaglandin-Endoperoxide Synthases, Solubility, Sulfonamides, Dinoprostone, Amyloid beta-Peptides, Inflammation Mediators, Mitogen-Activated Protein Kinases, Myocytes, Smooth Muscle, p38 Mitogen-Activated Protein Kinases, Rats, Cyclooxygenase 2, In Vitro Techniques
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