ArticleInternational journal of radiation oncology, biology, physics2010
Activation of protease activated receptor 2 by exogenous agonist exacerbates early radiation injury in rat intestine.
Article in International journal of radiation oncology, biology, physics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Proteinase-Activated Receptor 2 (PAR2) Deficiency and Cardiovascular Regulation: Context-Dependent Effects on Inflammation and Fibrosis.Current issues in molecular biology · 2026Review
- Protease-activated receptors (PARs)--biology and role in cancer invasion and metastasis.Cancer metastasis reviews · 2015Review
- Carbon Ion Irradiated Neural Injury Induced the Peripheral Immune Effects in Vitro or in Vivo.International journal of molecular sciences · 2015Article
- Targeting proteinase-activated receptors: therapeutic potential and challenges.Nature reviews. Drug discovery · 2012Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeProtease-activated receptor-2 (PAR(2)) is highly expressed throughout the gut and regulates the inflammatory, mitogenic, fibroproliferative, and nociceptive responses to injury. PAR(2) is strikingly upregulated and exhibits increased activation in response to intestinal irradiation. We examined the mechanistic significance of radiation enteropathy development by assessing the effect of exogenous PAR(2) activation. METHODS AND MATERIALS: Rat small bowel was exposed to localized single-dose radiation (16.5 Gy). The PAR(2) agonist (2-furoyl-LIGRLO-NH(2)) or vehicle was injected intraperitoneally daily for 3 days before irradiation (before), for 7 days after irradiation (after), or both 3 days before and 7 days after irradiation (before-after). Early and delayed radiation enteropathy was assessed at 2 and 26 weeks after irradiation using quantitative histologic examination, morphometry, and immunohistochemical analysis.
resultsThe PAR(2) agonist did not elicit changes in the unirradiated (shielded) intestine. In contrast, in the irradiated intestine procured 2 weeks after irradiation, administration of the PAR(2) agonist was associated with more severe mucosal injury and increased intestinal wall thickness in all three treatment groups (p <.05) compared with the vehicle-treated controls. The PAR(2) agonist also exacerbated the radiation injury score, serosal thickening, and mucosal inflammation (p <.05) in the before and before-after groups. The short-term exogenous activation of PAR(2) did not affect radiation-induced intestinal injury at 26 weeks.
conclusionThe results of the present study support a role for PAR(2) activation in the pathogenesis of early radiation-induced intestinal injury. Pharmacologic PAR(2) antagonists might have the potential to reduce the intestinal side effects of radiotherapy and/or as countermeasures in radiologic accidents or terrorism scenarios.
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Registered trials
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