ArticlePeptides2014
Urocortin 3 expression at baseline and during inflammation in the colon: corticotropin releasing factor receptors cross-talk.
Article in Peptides, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review.Journal of neuroinflammation · 2020Pooled it
- Review
- Mast cell corticotropin-releasing factor subtype 2 suppresses mast cell degranulation and limits the severity of anaphylaxis and stress-induced intestinal permeability.The Journal of allergy and clinical immunology · 2019Article
- Urocortin 3 Levels Are Impaired in Overweight Humans With and Without Type 2 Diabetes and Modulated by Exercise.Frontiers in endocrinology · 2019Article
- Sexually dimorphic metabolic responses mediated by CRFBiology of sex differences · 2018Article
- Gastric corticotropin-releasing factor influences mast cell infiltration in a rat model of functional dyspepsia.PloS one · 2018Article
- Frontline Science: Corticotropin-releasing factor receptor subtype 1 is a critical modulator of mast cell degranulation and stress-induced pathophysiology.Journal of leukocyte biology · 2017Article
- Actin cytoskeleton-dependent regulation of corticotropin-releasing factor receptor heteromers.Molecular biology of the cell · 2017Article
- Sex- and corticotropin-releasing factor receptor 2- dependent actions of urocortin 1 during inflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Urocortins and CRF receptor type 2 variants in the male rat colon: gene expression and regulation by endotoxin and anti-inflammatory effect.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Endogenous CRF in rat large intestine mediates motor and secretory responses to stress.Neurogastroenterology and motility · 2016Article
- Corticotropin-Releasing Factor and Toll-Like Receptor Gene Expression Is Associated with Low-Grade Inflammation in Irritable Bowel Syndrome Patients with Depression.Gastroenterology research and practice · 2016Article
- Corticotropin-Releasing Hormone Receptor 2 Gene Variants in Irritable Bowel Syndrome.PloS one · 2016Article
- Role of Corticotropin-releasing Factor Signaling in Stress-related Alterations of Colonic Motility and Hyperalgesia.Journal of neurogastroenterology and motility · 2015Article
- Multi-facets of Corticotropin-releasing Factor in Modulating Inflammation and Angiogenesis.Journal of neurogastroenterology and motility · 2015Article
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
Urocortins (Ucn1-3), members of the corticotropin-releasing factor (CRF) family of neuropeptides, are emerging as potent immunomodulators. Localized, cellular expression of Ucn1 and Ucn2, but not Ucn3, has been demonstrated during inflammation. Here, we investigated the role of Ucn3 in a rat model of Crohn's colitis and the relative contribution of CRF receptors (CRF1 and CRF2) in regulating Ucn3 expression at baseline and during inflammation. Ucn3 mRNA and peptide were ubiquitously expressed throughout the GI tract in naïve rats. Ucn3 immunoreactivity was seen in epithelial cells and myenteric neurons. On day 1 of colitis, Ucn3 mRNA levels decreased by 80% and did not recover to baseline even by day 9. Next, we ascertained pro- or anti-inflammatory actions of Ucn3 during colitis. Surprisingly, unlike observed anti-inflammatory actions of Ucn1, exogenous Ucn3 did not alter histopathological outcomes during colitis and neither did it alter levels of pro-inflammatory cytokines IL-6 and TNF-α. At baseline, colon-specific knockdown of CRF1, but not CRF2 decreased Ucn3 mRNA by 78%, whereas during colitis, Ucn3 mRNA levels increased after CRF1 knockdown. In cultured cells, co-expression of CRF1+CRF2 attenuated Ucn3-stimulated intracellular Ca(2+) peak by 48% as compared to cells expressing CRF2 alone. Phosphorylation of p38 kinase increased by 250% during colitis and was significantly attenuated after Ucn3 administration. Thus, our results suggest that a balanced and coordinated expression of CRF receptors is required for proper regulation of Ucn3 at baseline and during inflammation.
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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.