منابع مشابه
Protease-activated receptor-2 modulates protease-activated receptor-1-driven neointimal hyperplasia.
OBJECTIVE Emerging evidence suggests that protease-activated receptors-1 and -2 (PAR1 and PAR2) can signal together in response to proteases found in the rapidly changing microenvironment of damaged blood vessels. However, it is unknown whether PAR1 and PAR2 promote or mitigate the hyperplastic response to arterial injury. Using cell-penetrating PAR1 pepducins and mice deficient in PAR1 or PAR2...
متن کاملPlasmin Activation of Glial Cells through Protease-Activated Receptor 1
The objective of this study was to determine whether plasmin could induce morphological changes in human glial cells via PAR1. Human glioblastoma A172 cells were cultured in the presence of plasmin or the PAR1 specific activating hexapeptide, SFLLRN. Cells were monitored by flow cytometry to detect proteolytic activation of PAR1 receptor. Morphological changes were recorded by photomicroscopy a...
متن کاملThrombin-Induced Calpain Activation Promotes Protease-Activated Receptor 1 Internalization
The serine protease thrombin activates Protease-Activated Receptors (PARs), a family of G-protein-coupled receptors (GPCRs) activated by the proteolytic cleavage of their extracellular N-terminal domain. Four members of this family have been identified: PAR1-4. The activation of Protease-Activated Receptor 1(PAR1), the prototype of this receptor family, leads to an increase in intracellular Ca+...
متن کاملKruppel-like factor 2 inhibits protease activated receptor-1 expression and thrombin-mediated endothelial activation.
OBJECTIVE The serine protease thrombin can dramatically alter endothelial gene expression in a manner that confers a proinflammatory phenotype. Recent studies have identified the Kruppel-like factor 2 (KLF2) as a critical regulator of endothelial gene expression. Herein, we provide evidence that KLF2 inhibits thrombin-mediated endothelial activation via alterations in expression of its principa...
متن کاملProtease-activated receptor-2 activation exaggerates TRPV1-mediated cough in guinea pigs.
A lowered threshold to the cough response frequently accompanies chronic airway inflammatory conditions. However, the mechanism(s) that from chronic inflammation results in a lowered cough threshold is poorly understood. Irritant agents, including capsaicin, resiniferatoxin, and citric acid, elicit cough in humans and in experimental animals through the activation of the transient receptor pote...
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ژورنال
عنوان ژورنال: The American Journal of Pathology
سال: 2006
ISSN: 0002-9440
DOI: 10.2353/ajpath.2006.050658