ArticleBMC neuroscience2007
Interleukin-3 prevents neuronal death induced by amyloid peptide.
Article in BMC neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 49 citations in OpenAlex.
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
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- Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025Review
- Abnormal Changes of IL3/IL3R and Its Downstream Signaling Pathways in the Prion-Infected Cell Line and in the Brains of Scrapie-Infected Rodents.Molecular neurobiology · 2024Article
- Interleukin-3 Modulates Macrophage Phagocytic Activity and Promotes Spinal Cord Injury Repair.CNS neuroscience & therapeutics · 2024Article
- Interleukin 3 Inhibits Glutamate-Cytotoxicity in Neuroblastoma Cell Line.Neurochemical research · 2024Article
- Exercised blood plasma promotes hippocampal neurogenesis in the Alzheimer's disease rat brain.Journal of sport and health science · 2024Article
- A glance through the effects of CD4Computational and structural biotechnology journal · 2023Review
- Interleukin-3 is associated with sTREM2 and mediates the correlation between amyloid-β and tau pathology in Alzheimer's disease.Journal of neuroinflammation · 2022Article
- Article
- Natural genetic variation determines microglia heterogeneity in wild-derived mouse models of Alzheimer's disease.Cell reports · 2021Article
- Cytokines and Soluble HLA-G Levels in the Acute and Recovery Phases of Arbovirus-Infected Brazilian Patients Exhibiting Neurological Complications.Frontiers in immunology · 2021Article
- Article
- Focus on the Role of Klotho Protein in Neuro-Immune Interactions in HT-22 Cells Upon LPS Stimulation.Cells · 2020Article
- Increased inflammation in BA21 brain tissue from African Americans with Alzheimer's disease.Metabolic brain disease · 2020Article
- The Pathway Coexpression Network: Revealing pathway relationships.PLoS computational biology · 2018Article
- Altered Gene Expression in Prefrontal Cortex of a Fabry Disease Mouse Model.Frontiers in molecular neuroscience · 2018Article
- Bi-directional Association of Cerebrospinal Fluid Immune Markers with Stage of Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2018Article
- Inflammatory Response in the CNS: Friend or Foe?Molecular neurobiology · 2017Review
- Glial cells are functionally impaired in juvenile neuronal ceroid lipofuscinosis and detrimental to neurons.Acta neuropathologica communications · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin-3 (IL-3) is an important glycoprotein involved in regulating biological responses such as cell proliferation, survival and differentiation. Its effects are mediated via interaction with cell surface receptors. Several studies have demonstrated the expression of IL-3 in neurons and astrocytes of the hippocampus and cortices in normal mouse brain, suggesting a physiological role of IL-3 in the central nervous system. Although there is evidence indicating that IL-3 is expressed in some neuronal populations, its physiological role in these cells is poorly known.
resultsIn this study, we demonstrated the expression of IL-3 receptor in cortical neurons, and analyzed its influence on amyloid beta (Abeta)-treated cells. In these cells, IL-3 can activate at least three classical signalling pathways, Jak/STAT, Ras/MAP kinase and the PI 3-kinase. Viability assays indicated that IL-3 might play a neuroprotective role in cells treated with Abeta fibrils. It is of interest to note that our results suggest that cell survival induced by IL-3 required PI 3-kinase and Jak/STAT pathway activation, but not MAP kinase. In addition, IL-3 induced an increase of the anti-apoptotic protein Bcl-2.
conclusionAltogether these data strongly suggest that IL-3 neuroprotects neuronal cells against neurodegenerative agents like Abeta.
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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.