The protease-activated receptor-3 (PAR-3) can signal autonomously to induce interleukin-8 release |
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Authors: | E. Ostrowska G. Reiser |
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Affiliation: | 1. Medizinische Fakult?t, Institut für Neurobiochemie, Otto-von-Guericke-Universit?t Magdeburg, Leipziger Strasse 44, 39120, Magdeburg, Germany
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Abstract: | Protease-activated receptors (PARs) play a clear role in the burst of inflammatory reactions and immune responses. However, for PAR-3, the most elusive member of the PAR family, the functional role is still largely unclear. It has been claimed that PAR-3 does not signal autonomously, although the wide expression of human PAR-3 indicates its important physiological roles. We demonstrate that in HEK-293 cells, stably transfected with human PAR-3, thrombin induced calcium signaling, IL-8 gene expression and IL-8 release. We confirmed this finding using human lung epithelial and human astrocytoma cells that express endogenous PAR-3. Moreover, thrombin exposure of HEK-293 cells resulted in ERK1/2 activation coinciding with IL-8 release. The effects of thrombin were not dependent on PAR-1 activation, as confirmed by PAR-1 gene silencing. Thus, we propose that PAR-3 is able to signal autonomously to induce IL-8 release mediated by ERK1/2 phosphorylation, which contributes actively to inflammatory responses. Received 9 December 2007; received after revision 16 January 2008; accepted 18 January 2008 |
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Keywords: | Protease-activated receptors epithelial cells interleukin-8 inflammatory mediators |
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