PROBLEM: The objectives of this study were to evaluate interleukin-1 (IL-1) binding and some postreceptor actions of this cytokine and tumor necrosis factor (TNF) in human myometrial cells (HMC). METHOD: Monolayer cultures of HMC were used to characterize binding and to measure cyclic (c)AMP, prostaglandin (PG)E2, and PGI2 production. Membrane preparations were used to assess ADP-ribosylation and for immunoblotting. RESULTS: HMC were found to specifically bind [125I]IL-1 with an apparent Kd of 2 x 10(-10) M. Incubation of HMC with IL-1 or TNF caused a time-dependent and dose-dependent accumulation of cAMP, as well as a significant potentiation of forskolin-promoted cAMP production. These cytokines also increase PGE2 and PGI2 output, independently of the activation of adenylyl cyclase. IL-1 treatment had no measurable effect either on cholera toxin-mediated and pertussis toxin-mediated ADP-ribosylation, or on the amount of Gi proteins, as assessed by immunoblotting using a polyclonal antibody. CONCLUSIONS: It is suggested that IL-1 and TNF may activate one or more isoforms of the catalytic component of adenylyl cyclase, raising intracellular cAMP.
PROBLEM: The objectives of this study were to evaluate interleukin-1 (IL-1) binding and some postreceptor actions of this cytokine and tumor necrosis factor (TNF) in human myometrial cells (HMC). METHOD: Monolayer cultures of HMC were used to characterize binding and to measure cyclic (c)AMP, prostaglandin (PG)E2, and PGI2 production. Membrane preparations were used to assess ADP-ribosylation and for immunoblotting. RESULTS: HMC were found to specifically bind [125I]IL-1 with an apparent Kd of 2 x 10(-10) M. Incubation of HMC with IL-1 or TNF caused a time-dependent and dose-dependent accumulation of cAMP, as well as a significant potentiation of forskolin-promoted cAMP production. These cytokines also increase PGE2 and PGI2 output, independently of the activation of adenylyl cyclase. IL-1 treatment had no measurable effect either on cholera toxin-mediated and pertussis toxin-mediated ADP-ribosylation, or on the amount of Gi proteins, as assessed by immunoblotting using a polyclonal antibody. CONCLUSIONS: It is suggested that IL-1 and TNF may activate one or more isoforms of the catalytic component of adenylyl cyclase, raising intracellular cAMP.
Authors: Pooja Mittal; Roberto Romero; Adi L Tarca; Sorin Draghici; Chia-Ling Nhan-Chang; Tinnakorn Chaiworapongsa; John Hotra; Ricardo Gomez; Juan Pedro Kusanovic; Deug-Chan Lee; Chong Jai Kim; Sonia S Hassan Journal: Am J Obstet Gynecol Date: 2011-02 Impact factor: 8.661
Authors: Pooja Mittal; Roberto Romero; Adi L Tarca; Juan Gonzalez; Sorin Draghici; Yi Xu; Zhong Dong; Chia-Ling Nhan-Chang; Tinnakorn Chaiworapongsa; Stephen Lye; Juan Pedro Kusanovic; Leonard Lipovich; Shali Mazaki-Tovi; Sonia S Hassan; Sam Mesiano; Chong Jai Kim Journal: J Perinat Med Date: 2010-07-14 Impact factor: 1.901
Authors: Jerome F Strauss; Roberto Romero; Nardhy Gomez-Lopez; Hannah Haymond-Thornburg; Bhavi P Modi; Maria E Teves; Laurel N Pearson; Timothy P York; Harvey A Schenkein Journal: Am J Obstet Gynecol Date: 2017-12-14 Impact factor: 8.661