PAF is a potent inflammatory mediator. Its in vivo effect is initiated by binding to its receptor on the target cell surface. In the present study, we develop a competitive PCR to quantitate PAF-R gene transcripts in rat tissues using a synthetic RNA as a competitor. We found that PAF-R mRNA is constitutively expressed in 5 tested organs, with the ileum containing the highest concentration ((3.49.+0.15) x 107 molecules/g RNA). Significant levels were also detected in the jejunum, spleen, lungs, and kidneys. We then examined the regulatory role of inflammatory mediators on PAF-R gene expression. PAF (1.5 w?/kg, iv) or LPS (5 mg /kg, iv) markedly increased ileal PAF-R mRNA. Moreover, PAF elicited a biphasic elevation of PAF-R mRNA within 6 h. The second phase was completely abolished by a PAF antagonist, and partially inhibited by anti-TNF antibody, indicating the involvement of endogenous PAF and TNF in this event. The effect of LPS was weaker than PAF, and only showed a monophasic response. We conclude that: (a) a preferential localization of PAF -R expression in the ileum, suggesting a role of PAF in intestinal inflammation; (b) an induction of PAF-R expression in vivo by its own agonist; (c) a complex regulation of PAF-R gene expression m vivo which involves a network of various inflammatory mediators.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology