ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014
Blockade of proteinase-activated receptor 4 inhibits neutrophil recruitment in experimental inflammation in mice.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Activation of the Coagulation Cascade as a Universal Danger Sign.Current issues in molecular biology · 2025Review
- Elevated protease-activated receptor 4 (PAR4) gene expression in Alzheimer's disease predicts cognitive decline.Neurobiology of aging · 2024Article
- Discovery of Protease-Activated Receptor 4 (PAR4)-Tethered Ligand Antagonists Using Ultralarge Virtual Screening.ACS pharmacology & translational science · 2024Article
- Role of protease-activated receptor 4 in mouse models of acute and chronic kidney injury.American journal of physiology. Renal physiology · 2024Article
- Review
- Platelets differentially modulate CD4Immunologic research · 2022Article
- Genetic deletion of platelet PAR4 results in reduced thrombosis and impaired hemostatic plug stability.Journal of thrombosis and haemostasis : JTH · 2022Article
- Protease-activated receptor 4 plays a role in lipopolysaccharide-induced inflammatory mechanisms in murine macrophages.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction.Circulation · 2020Article
- Thrombin receptor PAR4 drives canonical NLRP3 inflammasome signaling in the heart.Basic research in cardiology · 2020Article
- Protease-activated receptor 4 protects mice from Coxsackievirus B3 and H1N1 influenza A virus infection.Cellular immunology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OBJECTIVE AND
designThe activation of proteinase-activated receptors (PARs) has been implicated in the development of important hallmarks of inflammation, including in vivo leukocyte recruitment; however, its role in the regulation of leukocyte migration in response to inflammatory stimuli has not been elucidated until now. Here, we examined the effects of the PAR4 antagonist YPGKF-NH 2 (tcY-NH2) on neutrophil recruitment in experimentally induced inflammation.
methodsBALB/c mice were intrapleurally injected with tcY-NH2 (40 ng/kg) prior to intrapleural injection of carrageenan (Cg) or neutrophil chemoattractant CXCL8; the number of infiltrating neutrophils was evaluated after 4 h, and KC production was assessed at different times after Cg injection. Neutrophil adhesion and rolling cells were studied using a brain circulation preparation 4 h after the Cg or CXCL8 challenge in tcY-NH2-treated mice.
resultsPAR4 blockade inhibited CXCL8- and Cg-induced neutrophil migration into the pleural cavity of BALB/c mice and reduced neutrophil rolling and adherence. Surprisingly, PAR4 blockade increased the level of KC in response to carrageenan.
conclusionThese results demonstrated that PAR4 blockade impairs neutrophil migration in vivo, suggesting that PAR4 plays an important role in the regulation of inflammation, at least in part because of its ability to inhibit the actions of the neutrophil chemoattractant CXCL8.
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Registered trials
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