Cited by 55Neuroinflammation and Neurodegeneration MechanismsParkinson's Disease Mechanisms and TreatmentsNuclear Receptors and Signaling

Upregulation of α‐synuclein by lipopolysaccharide and interleukin‐1 in human macrophages

Tanji, Kunikazu, Mori, Fumiaki, Imaizumi, Tadaatsu, Yoshida, Hidemi, Matsumiya, Tomoh, Tamo, Wakako, Yoshimoto, Makoto, Odagiri, Hiroki +4 more·2002·Pathology International

Abstract

α‐Synuclein was originally identified as the presynaptic nerve terminal protein. Recently, we reported that α‐synuclein is also expressed in cultured human astrocytes and that its levels are increased by stimulation with interleukin‐1β, suggesting that it may be involved in inflammatory processes. We therefore investigated the effect of inflammatory stimuli on α‐synuclein expression in human macrophages. α‐Synuclein mRNA and protein were detected in cultured human macrophages and levels of α‐synuclein protein were increased by stimulation with lipopolysaccharide and interleukin‐1β in a time‐ and concentration‐dependent manner. Immunofluorescent staining showed that α‐synuclein protein was expressed within the cytoplasm and nucleus. Furthermore, α‐synuclein immunoreactivity was present in alveolar macrophages from human lung tissues. These findings suggest that the function of α‐synuclein is not exclusive to the nervous system and that α‐synuclein may play a role in inflammatory processes and immune responses.

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Crossref · 10.1046/j.1440-1827.2002.01385.x

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  • Endotoxin increases α-synuclein production by macrophages and drives α-synuclein fibrillization.

    “Endotoxin increases α-synuclein production by macrophages [100] and drives α-synuclein fibrillization [70, 71].”

    From The endotoxin hypothesis of neurodegeneration (2019) · cites this paper as [100]

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Authors
Tanji, K., Mori, F., Imaizumi, T., Yoshida, H., Matsumiya, T., Tamo, W., Yoshimoto, M., Odagiri, H., Sasaki, M., Takahashi, H., Satoh, K., & Wakabayashi, K.
Affiliations
  • Hirosaki University (JP)
  • Taisho Pharmaceutical (Japan) (JP)
  • Brain Research Institute, Niigata University (JP)
Corresponding author
Tanji, Kunikazu
Venue
Pathology International
Publisher
Wiley
Published
2002-09
Volume
52
Issue
9
Pages
572-577
ISSN
  • 1320-5463 (ISSN-L)
  • 1440-1827
OpenAlex
W2050991927
Cited by
55
References
24
Citations by year
2024: 1 · 2023: 1 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 1
FWCI
1.93
Type
journal article
Language
en
Open access
closed
Locations
  • Pathology International (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Naito Foundation
  • Uehara Memorial Foundation
  • Fondation pour la Recherche Médicale
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
alpha-synuclein, lipopolysaccharide, IL-1β, human macrophages, alveolar macrophages, neuroinflammation, gene upregulation, inflammatory stimuli, immune response, subcellular localization
MeSH terms
Cells, Cultured, Dose-Response Relationship, Drug, Fluorescent Antibody Technique, Humans, Immunohistochemistry, Interleukin-1, Lipopolysaccharides, Lung, Macrophages, Nerve Tissue Proteins, Proteins, RNA, Messenger, Blotting, Western, Up-Regulation, Macrophages, Alveolar, Synucleins, alpha-Synuclein

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