American journal of reproductive immunology (New York, N.Y. : 1989) · 2001
Interleukin-1beta-induced prostaglandin E2 production in human myometrial cells: role of a pertussis toxin-sensitive component.
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Hertelendy F, Rastogi P, Molnár M, Romero R
Аннотация
PROBLEM: The objective of this study was to evaluate the possible role of pertussis toxin (PTX)-sensitive G-protein(s) in interleukin-1beta (IL-1) signaling in human myometrial cells (HMC).
METHOD: Primary cultures of HMC were stimulated with human recombinant IL-1 alone or in combination with PTX. Prostaglandin (PG) E2 in the medium was measured by radioimmunoassay, cyclooxygenase type 2 (Cox-2) and IkappaB by western analysis, and the activities of two members of the mitogen-activated protein kinase (MAPK) family of enzymes, ERK-2 and JNK, by the phosphorylation of appropriate substrates.
RESULTS: IL-1 increased PGE2 output during an 18-hr long incubation by 21.7-fold (n = 5 experiments). This increase was inhibited by 57% after pretreatment overnight with PTX. IL-1-induced expression of Cox-2 protein was also suppressed to a similar degree in PTX-treated HMC cultures. Degradation of the nuclear factor kappa B (NF-kappaB)-inhibiting protein (IkappaB), a critical step in IL-1 signaling to the nucleus, was significantly inhibited by PTX, as was IL-1-induced activation of ERK-2 and JNK.
CONCLUSIONS: It is suggested that the occupied IL-1 receptor-generated signal in HMC is transmitted by multiple pathways. One is coupled to a PTX-sensitive G-protein upstream from the MAPK phosphorylation cascade. This, in turn, may interact with another signaling pathway, the activation of NF-kappaB, via the phosphorylation of the IkappaB kinase complex.
METHOD: Primary cultures of HMC were stimulated with human recombinant IL-1 alone or in combination with PTX. Prostaglandin (PG) E2 in the medium was measured by radioimmunoassay, cyclooxygenase type 2 (Cox-2) and IkappaB by western analysis, and the activities of two members of the mitogen-activated protein kinase (MAPK) family of enzymes, ERK-2 and JNK, by the phosphorylation of appropriate substrates.
RESULTS: IL-1 increased PGE2 output during an 18-hr long incubation by 21.7-fold (n = 5 experiments). This increase was inhibited by 57% after pretreatment overnight with PTX. IL-1-induced expression of Cox-2 protein was also suppressed to a similar degree in PTX-treated HMC cultures. Degradation of the nuclear factor kappa B (NF-kappaB)-inhibiting protein (IkappaB), a critical step in IL-1 signaling to the nucleus, was significantly inhibited by PTX, as was IL-1-induced activation of ERK-2 and JNK.
CONCLUSIONS: It is suggested that the occupied IL-1 receptor-generated signal in HMC is transmitted by multiple pathways. One is coupled to a PTX-sensitive G-protein upstream from the MAPK phosphorylation cascade. This, in turn, may interact with another signaling pathway, the activation of NF-kappaB, via the phosphorylation of the IkappaB kinase complex.