ArticleNeurochemical research2003
S100B protein and 4-hydroxynonenal in the spinal cord of wobbler mice.
Article in Neurochemical research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 19 citations in OpenAlex.
- Distribution and time-course of 4-hydroxynonenal, heat shock protein 110/105 family members and cyclooxygenase-2 expression in the hippocampus of rat during trimethyltin-induced neurodegeneration.Neurochemical research · 2011Article
- Stage dependent effects of progesterone on motoneurons and glial cells of wobbler mouse spinal cord degeneration.Cellular and molecular neurobiology · 2010Article
- Don't fence me in: harnessing the beneficial roles of astrocytes for spinal cord repair.Restorative neurology and neuroscience · 2008Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100B is a calcium-binding protein that, in the nervous system, is mainly concentrated in glial cells. Although its biological role is still unclear, the protein is hypothesized, at high concentrations, to act in the pathogenesis of neurodegenerative processes, possibly through oxidative stress mechanisms. To investigate this hypothesis we studied the spinal cord of wobbler mice, an animal model of motor neuron degeneration. Using immunocytochemistry, we detected an overexpression of S100B in astrocytes of the cervical spinal cord of these animals. We also confirmed this finding by reverse transcriptase polymerase chain reaction. In the same spinal cord regions, scattered neurons appeared to be immunostained for 4-hydroxynonenal-modified proteins, an indicator of lipid peroxidation. This finding constitutes a sign of oxidative stress-induced neurodegeneration.
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Registered trials
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