Abstract：
OBJECTIVE: Although the functions of progesterone in the myometrium are well-established, the nongenomic effects of progesterone in pregnant myometrial contractions are still unclear. Therefore, this study aimed to investigate changes in the nongenomic effects of progesterone during pregnancy.
METHODS: Myometrial strips were obtained from non-pregnant, pregnant, and postpartum rats, and the nongenomic effects of progesterone in the myometrium during pregnancy were examined. Additionally, the influence of actinomycin D and cycloheximide and the effects of Org OD-02-0 (a specific membrane progesterone receptor (mPR) agonist) in the myometrium were investigated. Moreover, DNA microarray and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to identify genes involved in progesterone-induced effects in the myometrium.
RESULTS: Progesterone did not cause rhythmic contractions in non-pregnant myometrium but induced rhythmic contractions in pregnant myometrium, with the effects peaking at 20 d + 8 h of pregnancy. However, myometrial contractions decreased after delivery and were restored to non-pregnant levels at 7 d postpartum. Additionally, progesterone stably inhibited high KCl-induced myometrial contractions during pregnancy. Moreover, the nongenomic effects of progesterone were unaffected by actinomycin D or cycloheximide, and Org OD-02-0 effectively mimicked these effects. DNA microarray analysis and qRT-PCR revealed a significant increase in mPRβ gene expression during pregnancy. However, mPRα, mPRγ, mPRδ, and mPRε expression levels remained unchanged.
CONCLUSIONS: The stimulatory nongenomic effect of progesterone, which was inducible and mPRβ-dependent during pregnancy, may be involved in parturition. The inhibitory effect, which was constitutive and depended on other mPRs, may be involved in pregnancy maintenance.
METHODS: Myometrial strips were obtained from non-pregnant, pregnant, and postpartum rats, and the nongenomic effects of progesterone in the myometrium during pregnancy were examined. Additionally, the influence of actinomycin D and cycloheximide and the effects of Org OD-02-0 (a specific membrane progesterone receptor (mPR) agonist) in the myometrium were investigated. Moreover, DNA microarray and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to identify genes involved in progesterone-induced effects in the myometrium.
RESULTS: Progesterone did not cause rhythmic contractions in non-pregnant myometrium but induced rhythmic contractions in pregnant myometrium, with the effects peaking at 20 d + 8 h of pregnancy. However, myometrial contractions decreased after delivery and were restored to non-pregnant levels at 7 d postpartum. Additionally, progesterone stably inhibited high KCl-induced myometrial contractions during pregnancy. Moreover, the nongenomic effects of progesterone were unaffected by actinomycin D or cycloheximide, and Org OD-02-0 effectively mimicked these effects. DNA microarray analysis and qRT-PCR revealed a significant increase in mPRβ gene expression during pregnancy. However, mPRα, mPRγ, mPRδ, and mPRε expression levels remained unchanged.
CONCLUSIONS: The stimulatory nongenomic effect of progesterone, which was inducible and mPRβ-dependent during pregnancy, may be involved in parturition. The inhibitory effect, which was constitutive and depended on other mPRs, may be involved in pregnancy maintenance.
摘要：
目的：虽然孕激素在子宫肌层中的功能已得到证实，孕激素在妊娠子宫肌层收缩中的非基因组效应尚不清楚.因此,本研究旨在探讨孕激素在妊娠期间的非基因组效应变化.
方法：子宫肌层条取自非孕妇，怀孕,产后老鼠，并检查了孕酮在妊娠期间子宫肌层的非基因组效应。此外,研究了放线菌素D和环己酰亚胺的影响以及OrgOD-02-0（一种特定的膜孕酮受体（mPR）激动剂）在子宫肌层中的作用。此外，进行DNA微阵列和定量实时聚合酶链反应（qRT-PCR）以鉴定参与孕酮诱导的子宫肌层作用的基因。
结果：孕酮不引起非妊娠子宫肌层的节律性收缩，但引起妊娠子宫肌层的节律性收缩，效果在怀孕20d+8h达到峰值。然而,分娩后子宫肌层收缩减少，产后7d恢复到非妊娠水平。此外,孕酮稳定抑制怀孕期间高KCl诱导的子宫肌层收缩。此外，黄体酮的非基因组效应不受放线菌素D或环己酰亚胺的影响，和OrgOD-02-0有效地模仿了这些效果。DNA微阵列分析和qRT-PCR显示，怀孕期间mPRβ基因表达显着增加。然而,mPRα,mPRγ,mPRδ,和mPRε表达水平保持不变。
结论：孕酮的刺激性非基因组效应，在怀孕期间是诱导型和mPRβ依赖性的，可能参与分娩。抑制作用，这是构成性的，并且依赖于其他mPRs，可能参与妊娠维持。
方法：子宫肌层条取自非孕妇，怀孕,产后老鼠，并检查了孕酮在妊娠期间子宫肌层的非基因组效应。此外,研究了放线菌素D和环己酰亚胺的影响以及OrgOD-02-0（一种特定的膜孕酮受体（mPR）激动剂）在子宫肌层中的作用。此外，进行DNA微阵列和定量实时聚合酶链反应（qRT-PCR）以鉴定参与孕酮诱导的子宫肌层作用的基因。
结果：孕酮不引起非妊娠子宫肌层的节律性收缩，但引起妊娠子宫肌层的节律性收缩，效果在怀孕20d+8h达到峰值。然而,分娩后子宫肌层收缩减少，产后7d恢复到非妊娠水平。此外,孕酮稳定抑制怀孕期间高KCl诱导的子宫肌层收缩。此外，黄体酮的非基因组效应不受放线菌素D或环己酰亚胺的影响，和OrgOD-02-0有效地模仿了这些效果。DNA微阵列分析和qRT-PCR显示，怀孕期间mPRβ基因表达显着增加。然而,mPRα,mPRγ,mPRδ,和mPRε表达水平保持不变。
结论：孕酮的刺激性非基因组效应，在怀孕期间是诱导型和mPRβ依赖性的，可能参与分娩。抑制作用，这是构成性的，并且依赖于其他mPRs，可能参与妊娠维持。
