PAF-induced kinin B1 receptor in vivo up-regulation: involvement of distinct kinase pathways
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Platelet activating factor (PAF) is an important mediator in several pathophysiological processes. PAF receptor activation can causes a series of cellular and tissuemodifications and can lead to the production and/or release of diverse molecules, including cytokines, chemokines and receptors, amongst others, which are capable of amplifying the inflammation. PAF can up-regulate kinin B1 receptor expression by various mechanisms. In the present study, we show an additional mechanism by which PAF can lead to an in vivo up-regulation of B1 receptors. Our results clearly show that the phosphorylation of both ERK1/2 and JNK MAPKinases is an important step for this event. However, the exact mechanisms (transcriptional and post- transcriptional) by which PAF can trigger kinase phosphorylation and then up-regulate the B1 receptor require further investigation.
KeywordsPlatelet Activate Factor SB203580 PD98059 Platelet Activate Factor Receptor Tribromoethanol
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