ArticleBrain research2008
Interleukin-1beta interferes with signal transduction induced by neurotrophin-3 in cortical neurons.
Article in Brain research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Supramolecular organizing centers at the interface of inflammation and neurodegeneration.Frontiers in immunology · 2022Review
- Neuroimmune System as a Driving Force for Plasticity Following CNS Injury.Frontiers in cellular neuroscience · 2020Review
- The Role of Neuronal NLRP1 Inflammasome in Alzheimer's Disease: Bringing Neurons into the Neuroinflammation Game.Molecular neurobiology · 2019Review
- Involvement of Akt/CREB signaling pathways in the protective effect of EPA against interleukin-1β-induced cytotoxicity and BDNF down-regulation in cultured rat hippocampal neurons.BMC neuroscience · 2018Article
- Interleukin-1 beta promotes neuronal differentiation through the Wnt5a/RhoA/JNK pathway in cortical neural precursor cells.Molecular brain · 2018Article
- A Logic Model of Neuronal-Glial Interaction Suggests Altered Homeostatic Regulation in the Perpetuation of Neuroinflammation.Frontiers in cellular neuroscience · 2018Article
- Nutritional and Pharmacological Strategies to Regulate Microglial Polarization in Cognitive Aging and Alzheimer's Disease.Frontiers in aging neuroscience · 2017Review
- Insulin receptor substrate-2 is expressed in kidney epithelium and up-regulated in diabetic nephropathy.The FEBS journal · 2013Article
- The pro-inflammatory cytokines IL-1β and TNFα are neurotrophic for enteric neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Absence of IL-1β positively affects neurological outcome, lesion development and axonal plasticity after spinal cord injury.Journal of neuroinflammation · 2013Article
- Interleukin-1β in Central Nervous System Injury and Repair.European journal of neurodegenerative disease · 2012Article
- BDNF-, IGF-1- and GDNF-secreting human neural progenitor cells rescue amyloid β-induced toxicity in cultured rat septal neurons.Neurochemical research · 2012Article
- Dysregulated neuronal-microglial cross-talk during aging, stress and inflammation.Experimental neurology · 2012Review
- Interleukin-1 beta and neurotrophin-3 synergistically promote neurite growth in vitro.Journal of neuroinflammation · 2011Article
- Role of microglia in ethanol's apoptotic action on hypothalamic neuronal cells in primary cultures.Alcoholism, clinical and experimental research · 2010Article
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 2 institutions in 2 countries.
Funding
Abstract
It was previously observed that IL-1beta interferes with BDNF-induced TrkB-mediated signal transduction and protection of cortical neurons from apoptosis evoked by deprivation from trophic support [Tong L., Balazs R., Soiampornkul R., Thangnipon W., Cotman C.W., 2007. Interleukin-1beta impairs brain derived neurotrophic factor-induced signal transduction. Neurobiol. Aging]. Here we investigated whether the effect of the cytokine on neurotrophin signaling is more general. The influence of IL-1beta on NT-3 signaling was therefore studied under conditions when NT-3 primarily activated the TrkC receptor. The cytokine reduced NT-3-induced activation of MAPK/ERK and Akt, but did not interfere with Trk receptor autophosphorylation. IL-1beta reduced tyrosine phosphorylation of the docking proteins, IRS-1 and Shc, which convey receptor activation to the downstream protein kinase cascades. These are the steps that are also inhibited by IL-1beta in BDNF-induced signal transduction. The functional consequences of the effect of IL-1beta on NT-3 signaling were severe, as NT-3 protection of the trophic support-deprived cortical neurons was abrogated. In view of the role in the maintenance and plasticity of neurons of ERK, Akt and CREB, which are activated by neurotrophins, elevated IL-1beta levels in the brain in Alzheimer's disease and other neurodegenerative diseases might contribute to the decline in cognitive functions before the pathological signs of the disease develop.
Indexed as
Identifiers
What OpenQuestion holds
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.