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Interleukin‐1β up‐regulates expression of neurofilament light in human neuronal cells
Author(s) -
Rempel Hans,
Kusdra Leonard,
Pulliam Lynn
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00439.x
Subject(s) - neurofilament , cytoskeleton , microglia , microbiology and biotechnology , biology , neurodegeneration , cytokine , nf κb , interleukin , tau protein , interleukin 6 , inflammation , alzheimer's disease , chemistry , pathology , immunology , signal transduction , cell , immunohistochemistry , medicine , disease , biochemistry
Elevated expression of interleukin‐1 (IL‐1β), a pro‐inflammatory cytokine secreted by activated microglia, is a pathogenic marker of numerous neurodegenerative processes including Alzheimer's disease (AD). We have characterized a link between IL‐1β and the 68‐kDa neurofilament light (NF‐L) protein, which is a major component of the neuronal cytoskeleton. Using human brain aggregate cultures, we found that IL‐1β treatment significantly increased NF‐L expression in primary neurons. Analysis of mRNA levels demonstrated elevated NF‐L expression within 72 h while imaging of neurons by immunofluorescent staining for NF‐L confirmed IL‐1β‐induced NF‐L protein expression. These observations suggest a potential inflammatory‐induced mechanism for deregulation of an important cytoskeletal protein, NF‐L, possibly leading to neuronal dysfunction.