ArticleBritish journal of pharmacology2005
Neutrophils and the kallikrein-kinin system in proteinase-activated receptor 4-mediated inflammation in rodents.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 93 citations in OpenAlex.
- Protease-activated receptors act as a liaison between metabolism and inflammation.Inflammopharmacology · 2026Review
- 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
- Protease-activated receptors in health and disease.Physiological reviews · 2023Review
- Therapeutic values of chick early amniotic fluid (ceAF) that facilitates wound healing via potentiating a SASP-mediated transient senescence.Genes & diseases · 2022Article
- Increased Mucosal Thrombin is Associated with Crohn's Disease and Causes Inflammatory Damage through Protease-activated Receptors Activation.Journal of Crohn's & colitis · 2021Article
- A Murine Skin Infection Model Capable of Differentiating the Dermatopathology of Community-Associated MRSA Strain USA300 from Other MRSA Strains.Microorganisms · 2021Article
- Pulmonary histopathology in fatal paraquat poisoning.Autopsy & case reports · 2021Article
- Using PAR4 Inhibition as an Anti-Thrombotic Approach: Why, How, and When?International journal of molecular sciences · 2019Review
- Edema Induced by aInternational journal of molecular sciences · 2018Article
- Skin neurogenic inflammation.Seminars in immunopathology · 2018Review
- The Plasma Kallikrein-Kininogen Pathway Is Critical in the Pathogenesis of Colitis in Mice.Frontiers in immunology · 2018Article
- Regulation of intestinal permeability: The role of proteases.World journal of gastroenterology · 2017Review
- Protease-activated receptor 4: from structure to function and back again.British journal of pharmacology · 2016Review
- Review
- Increased expression of protease-activated receptor 2 and 4 within dorsal root ganglia in a rat model of bone cancer pain.Journal of molecular neuroscience : MN · 2015Article
- New insights into protease-activated receptor 4 signaling pathways in the pathogenesis of inflammation and neuropathic pain: a literature review.Channels (Austin, Tex.) · 2015Review
- Blockade of proteinase-activated receptor 4 inhibits neutrophil recruitment in experimental inflammation in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 We evaluated a potential role for proteinase-activated receptor 4 (PAR(4)) in a rodent paw inflammation model, with a focus on two main features of inflammation: (1) oedema and (2) granulocyte recruitment. 2 A PAR(4) antagonist (Pepducin P4pal-10; palmitoyl-SGRRYGHALR-NH(2)) reduced both the oedema and granulocyte recruitment induced by a localized administration of carrageenan in the rat hind paw, pointing to a key role for PAR(4) in this inflammation model. 3 Further, intraplantar injection in the mouse hind paw of a PAR(4) agonist (AYPGKF-NH(2)), but not its standard PAR(4)-inactive peptide control (YAPGKF-NH(2)), caused an inflammatory reaction characterized by oedema (increased paw thickness) and granulocyte recruitment (increased paw myeloperoxidase activity). The PAR(4) agonist-induced effects were inhibited in mice pretreated with pepducin P4pal10. 4 These PAR(4) agonist-mediated effects were not affected by pretreatment with inhibitors of either NO production or prostaglandin release (L-NAME and indomethacin, respectively). 5 However, selective immuno-depletion of neutrophils significantly reduced PAR(4) agonist-induced oedema formation. 6 Moreover, AYPGKF-NH(2)-induced oedema was also reduced by pretreatment with either a kinin B(2) receptor antagonist (icatibant) or a tissue or plasma kallikrein inhibitor (FE999024 and FE999026, respectively), but not with a kinin B(1) receptor antagonist (SSR240612). 7 We conclude: (1) that PAR(4) plays an important role in the inflammatory response as it mediates some of the hallmarks of inflammation and (2) that PAR(4)-mediated oedema is dependent on the recruitment of neutrophils and components of the kallikrein-kinin system.
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