Induction of the bradykinin B2-receptor, but not of the bradykinin B1-receptor, by interleukin-1beta in cultivated human decidua-derived cells.
Aspects of the pathophysiological steps leading to preterm labor after intrauterine infection can be studied in a cell culture model of decidua-derived cells. In this model, bradykinin (BK) increases the release of arachidonic acid (AA), the precursor of labor-promoting prostaglandins. The release is more than additively increased when cells are pretreated with interleukin-1beta (IL-1beta). Binding studies indicate that the expression of the bradykinin B2-receptor (B2R) protein rises to up to 300% of control after incubation with IL-1beta for 24 h. Thus, there is an increased capacity of mediating the response to BK. These findings suggest a pivotal role for the kallikrein-kinin system (KKS) during labor caused by intrauterine infection. However, there was no binding to the bradykinin B1-receptor (B1R), and it could not be induced by IL-1R, which is a unique finding compared with other cell systems.
Rehbock
J
J
I. Frauenklinik, Ludwig-Maximilians-Universität München, Germany.
Miska
K
K
Buchinger
P
P
D016718:Arachidonic Acid / Q000378:metabolism; D002478:Cells, Cultured; D003656:Decidua / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D007752:Obstetric Labor, Premature / Q000209:etiology / Q000628:therapy; D011247:Pregnancy; D043783:Receptor, Bradykinin B1; D043782:Receptor, Bradykinin B2; D018002:Receptors, Bradykinin / Q000096:biosynthesis / Q000187:drug effects*
D007375:Interleukin-1; D043783:Receptor, Bradykinin B1; D043782:Receptor, Bradykinin B2; D018002:Receptors, Bradykinin; D016718:Arachidonic Acid