ArticleSurgery2008
Effects of ghrelin on neuronal survival in cells derived from dorsal motor nucleus of the vagus.
Article in Surgery, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 23 citations in OpenAlex.
- Vagus nerve stimulation to augment recovery from severe traumatic brain injury impeding consciousness: a prospective pilot clinical trial.Neurological research · 2013Trial
- Obligatory Activation of SRC and JNK by GDNF for Survival and Axonal Outgrowth of Postnatal Intestinal Neurons.Cellular and molecular neurobiology · 2022Article
- Altered physiology of gastrointestinal vagal afferents following neurotrauma.Neural regeneration research · 2021Review
- Article
- Live and heat-killed probiotic: effects on chronic experimental colitis induced by dextran sulfate sodium (DSS) in rats.International journal of clinical and experimental medicine · 2015Article
- TNFα causes thrombin-dependent vagal neuron apoptosis in inflammatory bowel disease.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2014Article
- Ghrelin attenuates brain injury after traumatic brain injury and uncontrolled hemorrhagic shock in rats.Molecular medicine (Cambridge, Mass.) · 2012Article
- Unraveling the link between leptin, ghrelin and different types of colitis.Annals of gastroenterology · 2011Review
- The hormone ghrelin prevents traumatic brain injury induced intestinal dysfunction.Journal of neurotrauma · 2010Article
- Stimulating the central nervous system to prevent intestinal dysfunction after traumatic brain injury.The Journal of trauma · 2010Article
- Integrating GHS into the Ghrelin System.International journal of peptides · 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 1 institution in 1 country.
Funding
Abstract
backgroundThe effects of intestinal inflammation on the central neurons projecting to the enteric nervous system are unknown. The dorsal motor nucleus of the vagus signals to the gastrointestinal system. Ghrelin is elevated in patients with inflammatory bowel disease and has been implicated as an inflammatory mediator. The purpose of this study was to investigate the effects of gastrointestinal inflammation on the dorsal motor nucleus of the vagus in rats, as well as the effects of proinflammatory cytokines and ghrelin on neurons from the dorsal motor nucleus of the vagus in vitro.
methodsDiI was injected into the stomach wall of rats to retrogradely label neurons of the dorsal motor nucleus of the vagus. Intestinal inflammation was induced with indomethacin injection. Serial serum ghrelin measurements were performed. Tissue was examined under fluorescent microscopy. In vitro studies using primary culture of neurons from the dorsal motor nucleus of the vagus were performed. Reverse transcriptase-polymerase chain reaction for cytokine transcripts and immunohistochemistry for cytokine receptors were performed. Cell proliferation and apoptosis were measured by enzyme-linked immunosorbent assay.
resultsA significant decrease of DiI labeling was demonstrated in the dorsal motor nucleus of the vagus of animals injected with indomethacin. Serum levels of ghrelin were significantly elevated 2 days after induction of inflammation. In vitro, apoptosis and cell proliferation were measured after 24-hour exposure to experimental conditions. Ghrelin alone had no effect on apoptosis. Exposure to interleukin (IL)-1 beta or tumor necrosis factor (TNF)-alpha increased apoptosis. The addition of ghrelin to cytokine resulted in significant decreases in apoptosis compared to cytokine alone. Ghrelin significantly increased neuronal proliferation. Exposure to IL-1 beta, IL-6, or TNF-alpha significantly decreased proliferation. The addition of ghrelin to TNF-alpha or IL-6 significantly increased cellular proliferation compared to cytokine alone.
conclusionsNeurons from the dorsal motor nucleus of the vagus that project to the stomach are reduced in number after induction of colitis in rats. In vitro, proinflammatory cytokines increase apoptosis and decrease cell proliferation of neurons from the dorsal motor nucleus of the vagus. These effects are attenuated by ghrelin.
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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.