PAR-1

AcronymDefinition
PAR-1Protease Activated Receptor Type 1
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It is reported that TERT-2 cells constitutively express high levels of PAR-1 and PAR-2 and lower level of PAR-3 [76], whereas human keratinocytes express PAR-2 [11], which can be upregulated by MMIF 77].
Like other "GPCRs," the PARs signal via a variety of G proteins: both PAR-1 [78] and PAR-2 [79] through [G[alpha].sub.q], [G[alpha].sub.i], [G[alpha].sub.12/13], and G[[beta].sub.[gamma]]; PAR-4 via [G[alpha].sub.q] and [G[alpha].sub.12/13] [78]; and PAR-3 via PAR-1 signaling by receptor dimerization.
Proteases mediating PAR-1 and PAR-2 activation differentially signal via MAPK cascades.
On the other hand, basolateral, but not apical, PAR-1 and PAR2 activation with selective agonists decreases transepithelial resistance (TER) and thereby facilitates neutrophil transepithelial migration [86].
It has been found that thrombin and a PAR-1 APs stimulate proliferation of HPBFs [68] and that thrombin and FoxO factors functionally interact through PI3K/Akt-dependent FoxO phosphorylation leading to vascular SMC proliferation [89].
It has been observed that thrombin, tryptase, elastase, and trypsin, as well as APs of PAR-1, -2, and -4, induce IL-8 [92] and MCP-1 [93] release from A549 cells, suggesting that the actions of thrombin and trypsin may be via PAR-1 and -4, and cell responses to tryptase, trypsin, and elastase may be through PAR2.
Agonists of PAR-1. Thrombin is able to mediate induction of IL-1[beta] and IL-6 cytokine production from PBMCs and PBMC cell proliferation in a PAR-1-dependent manner [47].
Human eosinophils express PAR-1 and -2, and PAR-2 is the major PAR receptor that is capable of modulating eosinophil function.
Potent heterocycle-based peptide-mimetic antagonists of PAR-1, RWJ-56110 [112], and RWJ-58259 [113] are potent, selective PAR-1 antagonists, which bind to PAR-1, interfere with calcium mobilization and cellular functions (platelet aggregation and cell proliferation), and do not affect PAR-2, -3, or -4.
It has been reported that thrombin is increased in nasal secretion of the patients with chronic rhinosinusitis and thrombin and PAR-1 APs stimulate VEGF secretion from cultured HAEC [98], suggesting that thrombin may play a role in nasal polyp formation by stimulating VEGF production from airway epithelial cells.
Heterozygous PAR-1 mice have less allergic inflammation but PAR-1 agonist worsens it.
It is observed that, in normal and asthmatic subjects, epithelial staining intensity of PAR-1 and PAR-3 is greater than that of PAR-4.