Modulation of kinin responses in human synovium by interleukin-1.
Bradykinin (BK) is a weak stimulus for prostaglandin E2 (PGE2) release in untreated human synovial cells, but a potent stimulus in interleukin-1 (IL-1) pretreated cells. The mechanism(s) by which IL-1 induces responsiveness of synovial cells to BK appears to be multifactorial. IL-1 not only upregulates the number of kinin receptors on these cells, but may also upregulate a calcium-dependent process involved in the synthesis of prostaglandins.
Bathon
J M
JM
Johns Hopkins University School of Medicine, Department of Medicine, Baltimore, MD.
Croghan
J E
JE
Goldman
D W
DW
MacGlashan
D W
DW
Proud
D
D
D001172:Arthritis, Rheumatoid / Q000378:metabolism*; D001920:Bradykinin / Q000378:metabolism* / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D015232:Dinoprostone / Q000378:metabolism*; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D007700:Kinetics; D018002:Receptors, Bradykinin; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D013582:Synovial Fluid / Q000166:cytology / Q000502:physiology
D007375:Interleukin-1; D018002:Receptors, Bradykinin; D017981:Receptors, Neurotransmitter; D011994:Recombinant Proteins; D015232:Dinoprostone; D001920:Bradykinin; D002118:Calcium