ArticleJournal of neuroscience research2008
Transcriptional profile of primary astrocytes expressing ALS-linked mutant SOD1.
Article in Journal of neuroscience research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Decorin Attenuates Epileptogenesis and Modulates Hippocampal Synaptic Plasticity via the mTOR Signalling Pathway.Neurochemical research · 2026Article
- Review
- PET imaging of reactive astrocytes in neurological disorders.European journal of nuclear medicine and molecular imaging · 2022Review
- Reactive astrocytes in ALS display diminished intron retention.Nucleic acids research · 2021Article
- Copper Dyshomeostasis in Neurodegenerative Diseases-Therapeutic Implications.International journal of molecular sciences · 2020Review
- Review
- Examining the relationship between astrocyte dysfunction and neurodegeneration in ALS using hiPSCs.Neurobiology of disease · 2019Review
- Phenotypic heterogeneity of astrocytes in motor neuron disease.Clinical & experimental neuroimmunology · 2018Review
- SOD1 Mutations Causing Familial Amyotrophic Lateral Sclerosis Induce Toxicity in Astrocytes: Evidence for Bystander Effects in a Continuum of Astrogliosis.Neurochemical research · 2018Article
- Role and Therapeutic Potential of Astrocytes in Amyotrophic Lateral Sclerosis.Current pharmaceutical design · 2017Review
- Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2015Article
- Deregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1(G93A) Amyotrophic Lateral Sclerosis mouse model.Frontiers in cellular neuroscience · 2014Article
- Investigating cell death mechanisms in amyotrophic lateral sclerosis using transcriptomics.Frontiers in cellular neuroscience · 2013Review
- Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability.Journal of neurophysiology · 2013Article
- Transcriptome Profiling Following Neuronal and Glial Expression of ALS-Linked SOD1 in Drosophila.G3 (Bethesda, Md.) · 2013Article
- Astrocyte pathology and the absence of non-cell autonomy in an induced pluripotent stem cell model of TDP-43 proteinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- The Nrf2-ARE pathway: a valuable therapeutic target for the treatment of neurodegenerative diseases.Recent patents on CNS drug discovery · 2012Review
- Upregulation of the E3 ligase NEDD4-1 by oxidative stress degrades IGF-1 receptor protein in neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Mechanisms of oxidative damage in multiple sclerosis and neurodegenerative diseases: therapeutic modulation via fumaric acid esters.International journal of molecular sciences · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is caused by the progressive degeneration of motor neurons. Mutations in the Cu/Zn superoxide dismutase (SOD1) are found in approximately 20% of patients with familial ALS. Mutant SOD1 causes motor neuron death through an acquired toxic property. Although the molecular mechanism underlying this toxic gain-of-function remains unknown, evidence support the role of mutant SOD1 expression in nonneuronal cells in shaping motor neuron degeneration. We have previously found that in contrast to nontransgenic cells, SOD1(G93A)-expressing astrocytes induced apoptosis of cocultured motor neurons. This prompted us to investigate whether the effect on motor neuron survival was related to a change in the gene expression profile. Through high-density oligonucleotide microarrays, we found changes in the expression of genes involved in transcription, signaling, cell proliferation, extracellular matrix synthesis, response to stress, and steroid and lipid metabolism. The most up-regulated gene was decorin (Dcn), a small multifunctional extracellular proteoglycan. Down-regulated genes included the insulin-like growth factor-1 receptor (Igf-1r) and the RNA binding protein ROD1. Rod1 was also found down-regulated in purified motor neurons expressing SOD1(G93A). Changes in the expression of Dcn, Igf-1r, and Rod1 were found in the spinal cord of asymptomatic animals, suggesting these changes occur before overt neuronal degeneration and potentially influence astrocyte-motor neuron interaction in the course of the disease. The astrocyte-specific gene expression profile might contribute to the identification of possible candidates for cell type-specific therapies in ALS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.