6-ketoprostaglandin-f1-alpha has been researched along with Uterine-Diseases* in 2 studies
2 other study(ies) available for 6-ketoprostaglandin-f1-alpha and Uterine-Diseases
| Article | Year |
|---|---|
Abnormal uterus with polycysts, accumulation of uterine prostaglandins, and reduced fertility in mice heterozygous for acyl-CoA synthetase 4 deficiency.
Arachidonate released by various stimuli is rapidly reesterified into membrane phospholipids initiated by acyl-CoA synthetase (ACS) and subsequent acyl-transfer reactions. ACS4 is an arachidonate-preferring enzyme abundant in steroidogenic tissues and postulated to modulate eicosanoid production. Female mice heterozygous for ACS4 deficiency become pregnant less frequently and produce small litters with extremely low transmission of the disrupted alleles. Striking morphological changes, including extremely enlarged uteri and lumina filled with numerous proliferative cysts of various sizes, were detected in ACS4+/- females. Furthermore, marked accumulation of prostaglandins was seen in the uterus of the heterozygous females. These results indicate that ACS4 modulates female fertility and uterine prostaglandin production. Topics: 6-Ketoprostaglandin F1 alpha; Animals; Chimera; Coenzyme A Ligases; Crosses, Genetic; Cysts; Dinoprost; Dinoprostone; Female; Genotype; Heterozygote; Infertility, Female; Litter Size; Male; Mice; Mice, Knockout; Mice, Transgenic; Prostaglandins; Restriction Mapping; Sex Ratio; Uterine Diseases; Uterus | 2001 |
Intrauterine infection and the effects of inflammatory mediators on prostaglandin production by myometrial cells from pregnant women.
Our purpose was to evaluate the effects of known stimulants of prostaglandin production on cultured myometrial cells from women in labor with and without intrauterine infection.. Myometrial segments were obtained from 16 patients between 33 and 40 weeks' gestation who had been in labor for > or = 8 hours at cesarean delivery; 8 patients had clinical chorioamnionitis and 8 did not. Myometrial cells were isolated and grown in culture. Incubations were conducted with interleukin-1 beta, tumor necrosis factor-alpha, or epidermal growth factor. Prostaglandin E2, prostaglandin F2 alpha, and 6-keto-prostaglandin F1 alpha (the stable metabolite of prostacyclin) were measured by radioimmunoassay, and cellular protein was determined.. Cultured human myometrial cells from patients with and without prior intrauterine infection produced prostaglandins in response to interleukin-1 beta, tumor necrosis factor-alpha, and epidermal growth factor at a significantly increased rate (p<0.05 vs controls at and above 10 ng/ml of interleukin-1 beta, tumor necrosis factor-alpha, and epidermal growth factor). The major prostaglandin produced in response to each stimulant was 6-keto-prostaglandin F1 alpha; however, this response was attenuated in cells from patients with intrauterine infection.. Cultured human myometrial cells from patients with and without prior intrauterine infection respond to known stimulants of prostaglandin production. Prior intrauterine infection has no effect on baseline prostaglandin production, but the amount of prostacyclin produced as a response to cellular stimulants is decreased with prior intrauterine infection. This effect may have a role in regulating myometrial function in intrauterine infection. Topics: 6-Ketoprostaglandin F1 alpha; Cells, Cultured; Cytokines; Dinoprost; Dinoprostone; Epidermal Growth Factor; Female; Humans; Infections; Interleukin-1; Myometrium; Pregnancy; Pregnancy Complications, Infectious; Prostaglandins; Tumor Necrosis Factor-alpha; Uterine Diseases | 1996 |