Induction of the bradykinin B2-receptor, but not of the bradykinin B1-receptor, by interleukin-1β in cultivated human decidua-derived cells

Kinin receptors in stimulated and characterized decidua tissue-derived cells

“…As shown previously, kinin B 1 receptors could not be induced by IL-1β in cultivated human decidua tissue-derived cells [21]. Here we confirmed this finding by equilibrium binding experiments, in situ RT-PCR and quantitative RT-PCR, and in addition examined the effect of bacterial lipopolysaccharide.…”

“…Taken together with the results obtained through receptor binding experiments, we conclude that decidual cells isolated and cultured did not express kinin B 1 receptor binding sites in measurable amounts above basal values in equilibrium binding experiments (equilibrium binding constant Kd N 50 nM) as it was shown for kinin B2 receptors (Kd = 0.85 nM, maximal binding capacity Bmax = 436 fmol/mg protein) in [2]. Rehbock et al [21] showed a comparable effect and report that in experiments with similar experimental design and conditions kinin B 2 receptors were the prominent mediators for the observed effects, e.g. the release of arachidonic acid in this tissue: Bradykinin but not des-Arg 9 -bradykinin together with IL-1β could increase the release of arachidonic acid, the precursor of prostaglandins.…”

“…In a combined action of IL-1β and bradykinin, but not with des-Arg 10 -bradykinin, an increased release of arachidonic acid can be observed in decidual cells [21]. Arachidonic acid is the precursor of labour-promoting prostaglandins [13].…”

“…These results show that bradykinin leads to an increased supply of arachidonic acid promoting the cyclooxygenase cascade and synthesis of labour promoting prostaglandins. The hypothesis of a concerted action of bradykinin and interleukin-1β (IL-1β) could be reinforced as the kinin B 2 receptor seems to be increasingly expressed after pre-treatment of the cells with IL-1β [21]. Bradykinin itself stimulates IL-6 and IL-8 secretion from human decidual cells, thereby initiating local and systemic effects of amniochorionitis [3].…”

Enhanced Ca2+ response and stimulation of prostaglandin release by the bradykinin B2 receptor in human retinal pigment epithelial cells primed with proinflammatory cytokines

“…These observations may explain why in some cellular systems cytokines have been reported to selectively upregulate the kinin B 2 receptor. Indeed IL-1b increased BK B 2 receptor expression and function in human bronchial airway smooth muscle cells, in canine tracheal smooth muscle cells and in human decidua-derived cells, without induction of the kinin B1-receptor [47,48,49]. Functionally, BK stimulated intracellular Ca 2+ mobilization and thereby produce a marked increase in COX-2-dependent PGE 2 release when administered following interleukin treatment [34,50,51].…”