ArticleNeural plasticity2016
Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress.
Article in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Heat Stress Modulates WDR5-Mediated H3K4me3 Modification to Induce Melanogenesis via Activating CX3CL1/CX3CR1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Rps27a might act as a controller of microglia activation in triggering neurodegenerative diseases.PloS one · 2020Article
- Intergenerational transmission of depression: clinical observations and molecular mechanisms.Molecular psychiatry · 2019Review
- Environment matters: microglia function and dysfunction in a changing world.Current opinion in neurobiology · 2017Review
- Exposure to gestational diabetes mellitus induces neuroinflammation, derangement of hippocampal neurons, and cognitive changes in rat offspring.Journal of neuroinflammation · 2017Article
- Proteomic Analysis of HDAC3 Selective Inhibitor in the Regulation of Inflammatory Response of Primary Microglia.Neural plasticity · 2017Article
- Retracted: Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress.Neural plasticityArticle
Corrections and comments
- Retraction · 2018-05-22Falsification/Fabrication of Image · Manipulation of Images ·
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The potential contribution of inflammation to the development of neuropsychiatric diseases has recently received substantial attention. In the brain, the main immune cells are the microglia. As they are the main source of inflammatory factors, it is plausible that the regulation of their activation may be a potential therapeutic target. Fractalkine (CX3CL1) and its receptor CX3CR1 play a crucial role in the control of the biological activity of the microglia. In the present study, using microglial cultures we investigated whether fractalkine is able to reverse changes in microglia caused by a prenatal stress procedure. Our study found that the microglia do not express fractalkine. Prenatal stress decreases the expression of the fractalkine receptor, which in turn is enhanced by the administration of exogenous fractalkine. Moreover, treatment with fractalkine diminishes the prenatal stress-induced overproduction of proinflammatory factors such as IL-1β, IL-18, IL-6, TNF-α, CCL2, or NO in the microglial cells derived from prenatally stressed newborns. In conclusion, the present results revealed that the pathological activation of microglia in prenatally stressed newborns may be attenuated by fractalkine administration. Therefore, understanding of the role of the CX3CL1-CX3CR1 system may help to elucidate the mechanisms underlying the neuron-microglia interaction and its role in pathological conditions in the brain.
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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.