ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2014
TNFα causes thrombin-dependent vagal neuron apoptosis in inflammatory bowel disease.
Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- RNA-Sequencing Reveals Gene Expression and Pathway Signatures in Umbilical Cord Blood Affected by Birth Delivery Mode.Phenomics (Cham, Switzerland) · 2023Article
- HMGB1 is a Potential and Challenging Therapeutic Target for Parkinson's Disease.Cellular and molecular neurobiology · 2023Review
- Gut microbiota composition modulates inflammation and structure of the vagal afferent pathway.Physiology & behavior · 2020Article
- Genetic mapping of cell type specificity for complex traits.Nature communications · 2019Article
- Brain TACE (Tumor Necrosis Factor-α-Converting Enzyme) Contributes to Sympathetic Excitation in Heart Failure Rats.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Baicalin Protects against Thrombin-Induced Cell Injury in Human Umbilical Vein Endothelial Cells.BioMed research international · 2019Article
- The Vagus Nerve in Appetite Regulation, Mood, and Intestinal Inflammation.Gastroenterology · 2017Review
- Baicalin protects against thrombin induced cell injury in SH-SY5Y cells.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe role of peripheral tumor necrosis factor alpha (TNFα) in inflammatory bowel disease (IBD) is well established, but its central nervous system (CNS) effects are not understood. Thrombin, another mediator of inflammation in IBD, has been implicated in CNS vagal neuron apoptosis in the dorsal motor nucleus of the vagus (DMV). This study evaluates DMV TNFα exposure, characterizes effects of TNFα on DMV neurons, and identifies a relationship between DMV TNFα and thrombin in IBD.
methods2,4,6-Trinitrobenzene sulfonic acid was administered via enema to induce colonic inflammation in rats. TNFα in serum, cerebrospinal fluid (CSF), and DMV tissues were determined by ELISA and DMV TNFα expression by quantitative reverse transcription PCR (RT-PCR). TNFα was administered into the fourth intracerebral ventricle (4 V) adjacent to the DMV, with and without blockade of TNF receptor 1 (TNFR1) and the thrombin receptor proteinase-activated receptor 1 (PAR1). Immunofluorescence was used to evaluate microglial activation (Cd11b) and prothrombin presence in DMV sections. Apoptosis was examined using terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) and activated caspase-3 immunofluorescence.
resultsIBD is associated with increased TNFα protein in serum, CSF, and DMV tissue; DMV TNFα transcription is also increased. TNFα (4 V) caused a 54 % increase in microglial activation, a 27 % increase in DMV prothrombin protein, and a 31 % increase in vagal neuron apoptosis by TUNEL. There was a 52 % increase in activated caspase-3 immunofluorescence in TNFα-treated animals (p < 0.05). All effects of 4 V TNFα were prevented by TNFR1 blockade. TNFα-induced apoptosis was prevented by PAR1 blockade.
conclusionsIBD is associated with DMV exposure to TNFα, causing excess DMV prothrombin and vagal apoptosis.
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