Amyloid β Protein Primes Cultured Rat Microglial Cells for an Enhanced Phorbol 12‐Myristate 13‐Acetate‐Induced Respiratory Burst Activity
Abstract
Activated microglia, often associated with neuritic amyloid plaques in the Alzheimer's disease brain, are likely to contribute to the progression of the disease process, e.g., by releasing neurotoxic reactive oxygen and/or nitrogen intermediates. In the present study, whether the amyloid beta peptide (A beta), the principal constituent of amyloid plaques, can stimulate microglial respiratory burst activity and/or microglial production of nitric oxide was examined. Using neonatal rat microglial cultures as a model, it was found that neither the spontaneous release of nitric oxide nor the lipopolysaccharide-induced production of nitric oxide was altered in cultures previously incubated with synthetic A beta (1-40) for 24 h. In addition, no direct stimulatory effect of A beta (1-40) on the respiratory burst activity was observed. Nevertheless, concomitant with an increase in the number of responsive cells, a profound priming of the phorbol 12-myristate 13-acetate-evoked production of superoxide anion was observed in A beta (1-40)-treated cultures. Thus, both the maximal rate and the total phorbol 12-myristate 13-acetate-induced production of superoxide appeared to be statistically significantly higher as compared with untreated cultures. It is concluded that, as far as activation of the microglial respiratory burst is concerned, A beta(1-40) may merely act as a priming rather than a triggering stimulus.
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Protein aggregation and neuronal damage result in activation of disease-associated microglia (DAM) via damage-associated molecular patterns (DAMPs).
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From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [27]
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- Authors
- Van Muiswinkel, F. L., Veerhuis, R., & Eikelenboom, P.
- Affiliations
- Vrije Universiteit Amsterdam (NL)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1996-06
- Volume
- 66
- Issue
- 6
- Pages
- 2468-2476
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1977917625
- Cited by
- 85
- References
- 0
- Citations by year
- 2025: 2 · 2024: 2 · 2020: 2 · 2019: 2 · 2016: 1 · 2014: 2 · 2012: 2
- FWCI
- 4.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Funders
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- amyloid-beta, microglia, respiratory burst, phorbol myristate acetate, superoxide, nitric oxide, microglial priming, Alzheimer's disease, reactive oxygen species, lipopolysaccharide, microglial activation
- MeSH terms
- Animals, Cells, Cultured, Dose-Response Relationship, Drug, Lipopolysaccharides, Nitric Oxide, Nitrites, Rats, Inbred Strains, Superoxides, Tetradecanoylphorbol Acetate, Amyloid beta-Peptides, Respiratory Burst, Microglia, Rats
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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 ›
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