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Upregulation of α‐synuclein by lipopolysaccharide and interleukin‐1 in human macrophages
Author(s) -
Tanji Kunikazu,
Mori Fumiaki,
Imaizumi Tadaatsu,
Yoshida Hidemi,
Matsumiya Tomoh,
Tamo Wakako,
Yoshimoto Makoto,
Odagiri Hiroki,
Sasaki Mutsuo,
Takahashi Hitoshi,
Satoh Kei,
Wakabayashi Koichi
Publication year - 2002
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1046/j.1440-1827.2002.01385.x
Subject(s) - alpha synuclein , lipopolysaccharide , downregulation and upregulation , alpha (finance) , stimulation , biology , cytoplasm , microbiology and biotechnology , synuclein , interleukin , messenger rna , tumor necrosis factor alpha , chemistry , immunology , pathology , parkinson's disease , cytokine , medicine , neuroscience , biochemistry , construct validity , nursing , disease , patient satisfaction , gene
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.