ArticleBritish journal of pharmacology2009
Urocortin promotes the development of vasculitis in a rat model of thromboangiitis obliterans via corticotrophin-releasing factor type 1 receptors.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 36 citations in OpenAlex.
- Role of CRH in colitis and colitis-associated cancer: a combinative result of central and peripheral effects?Frontiers in endocrinology · 2024Review
- Baiying qingmai formulation ameliorates thromboangiitis obliterans by inhibiting HMGB1/RAGE/NF-κB signaling pathways.Frontiers in pharmacology · 2022Article
- Molecular mechanisms regulating immune responses in thromboangiitis obliterans: A comprehensive review.Iranian journal of basic medical sciences · 2019Review
- Levistilide A Ameliorates NLRP3 Expression Involving the Syk-p38/JNK Pathway and Peripheral Obliterans in Rats.Mediators of inflammation · 2018Article
- Effect of omega-3 fatty acids on haemostatic functions in urocortin-treated obese rats.Journal of physiology and biochemistry · 2014Article
- Article
- Systemic administration of urocortin after intracerebral hemorrhage reduces neurological deficits and neuroinflammation in rats.Journal of neuroinflammation · 2012Article
- Clinical perspectives of urocortin and related agents for the treatment of cardiovascular disease.International journal of endocrinology · 2012Article
- Corticotropin-releasing factor family and its receptors: pro-inflammatory or anti-inflammatory targets in the periphery?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Review
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12 authors at 1 institution in 1 country.
Funding
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Abstract
background and purposeUrocortin is a locally expressed pro-inflammatory peptide. Here we have examined the effects of urocortin on sodium laurate-induced peripheral arterial vasculitis in rats, modelling the mechanisms of thromboangiitis obliterans (TAO). EXPERIMENTAL APPROACH: Peripheral vasculitis in rats was induced by sodium laurate and graded by gross appearance on the 12th day after injection. Histological changes in rat femoral arteries were assessed by histopathology and transmission electron microscopy. Blood cell counts, blood rheology, blood coagulation and plasma urocortin, thromboxane B(2), prostaglandin E(2) and soluble intercellular adhesion molecule-1 levels were measured. Expression of urocortin, corticotrophin-releasing factor (CRF(1/2)) receptors, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1) at both mRNA and protein levels were determined by RT-PCR and Western blot. KEY
resultsRats showed grossly visible signs and symptoms of TAO on the 12th day after sodium laurate injection. In these rats, blood was in a hypercoagulable state; plasma urocortin, prostaglandin E(2) and soluble intercellular adhesion molecule-1 levels were elevated; and the expression of urocortin, CRF(1) and CRF(1alpha)-receptors, COX-2 and ICAM-1 in rat femoral arteries were markedly increased. Exogenous urocortin, given for 12 days after sodium laurate, exacerbated the hypercoagulable state and augmented expression of CRF(1alpha)-receptors, COX-2 and ICAM-1. These effects were abolished by a CRF(1)-receptor antagonist, NBI-27914, or a non-selective CRF-receptor antagonist, astressin, but not by the CRF(2)-receptor antagonist, antisauvagine-30, given with exogenous urocortin. CONCLUSION AND IMPLICATIONS: Urocortin exacerbated the hypercoagulable state and vasculitis in a model of TAO induced by sodium laurate in rats, via CRF(1)-receptors. COX-2 and ICAM-1 might also have contributed to this exacerbation.
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