ArticlePloS one2012
Male-specific differences in proliferation, neurogenesis, and sensitivity to oxidative stress in neural progenitor cells derived from a rat model of ALS.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 43 citations in OpenAlex.
- Comorbidities in spinal muscular atrophy and their impact on the course of the underlying disease: a real-life observational study.BMC musculoskeletal disorders · 2025Observational
- SOD1-related inherited peripheral neuropathies in a Japanese cohort: genetic variants and clinical insights.Journal of neurology · 2025Article
- No significant sex differences in incidence or phenotype for the SMNΔ7 mouse model of spinal muscular atrophy.Neuromuscular disorders : NMD · 2024Article
- A distinct circular DNA profile intersects with proteome changes in the genotoxic stress-related hSOD1Cell & bioscience · 2023Article
- Modeling sex differences in humans using isogenic induced pluripotent stem cells.Stem cell reports · 2022Article
- Network Analysis Identifies Sex-Specific Gene Expression Changes in Blood of Amyotrophic Lateral Sclerosis Patients.International journal of molecular sciences · 2021Article
- Spinal muscular atrophy: Broad disease spectrum and sex-specific phenotypes.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Genetics and Sex in the Pathogenesis of Amyotrophic Lateral Sclerosis (ALS): Is There a Link?International journal of molecular sciences · 2020Review
- Sex differences in the response to oxidative and proteolytic stress.Redox biology · 2020Review
- The Role of Sex and Sex Hormones in Neurodegenerative Diseases.Endocrine reviews · 2020Review
- Mitochondrial Dysfunction, Neurogenesis, and Epigenetics: Putative Implications for Amyotrophic Lateral Sclerosis Neurodegeneration and Treatment.Frontiers in neuroscience · 2020Review
- Article
- Sex-Specific Differences in Redox Homeostasis in Brain Norm and Disease.Journal of molecular neuroscience : MN · 2019Review
- Implications of white matter damage in amyotrophic lateral sclerosis (Review).Molecular medicine reports · 2017Review
- Amyotrophic lateral sclerosis patient iPSC-derived astrocytes impair autophagy via non-cell autonomous mechanisms.Molecular brain · 2017Article
- Mitochondrial maintenance failure in aging and role of sexual dimorphism.Archives of biochemistry and biophysics · 2015Review
- Dietary lipid unsaturation influences survival and oxidative modifications of an amyotrophic lateral sclerosis model in a gender-specific manner.Neuromolecular medicine · 2014Article
- Adenosine monophosphate-activated protein kinase activation enhances embryonic neural stem cell apoptosis in a mouse model of amyotrophic lateral sclerosis.Neural regeneration research · 2014Article
- Focal transplantation of human iPSC-derived glial-rich neural progenitors improves lifespan of ALS mice.Stem cell reports · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive motor dysfunction and the loss of large motor neurons in the spinal cord and brain stem. A clear genetic link to point mutations in the superoxide dismutase 1 (SOD1) gene has been shown in a small group of familial ALS patients. The exact etiology of ALS is still uncertain, but males have consistently been shown to be at a higher risk for the disease than females. Here we present male-specific effects of the mutant SOD1 transgene on proliferation, neurogenesis, and sensitivity to oxidative stress in rat neural progenitor cells (rNPCs). E14 pups were bred using SOD1(G93A) transgenic male rats and wild-type female rats. The spinal cord and cortex tissues were collected, genotyped by PCR using primers for the SOD1(G93A) transgene or the male-specific Sry gene, and cultured as neurospheres. The number of dividing cells was higher in male rNPCs compared to female rNPCs. However, SOD1(G93A) over-expression significantly reduced cell proliferation in male cells but not female cells. Similarly, male rNPCs produced more neurons compared to female rNPCs, but SOD1(G93A) over-expression significantly reduced the number of neurons produced in male cells. Finally we asked whether sex and SOD1(G93A) transgenes affected sensitivity to oxidative stress. There was no sex-based difference in cell viability after treatment with hydrogen peroxide or 3-morpholinosydnonimine, a free radical-generating agent. However, increased cytotoxicity by SOD1(G93A) over-expression occurred, especially in male rNPCs. These results provide essential information on how the mutant SOD1 gene and sexual dimorphism are involved in ALS disease progression.
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Registered trials
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