Andersson Stefan, Minjarez Debra, Yost Nicole P, Word R Ann
Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9032, USA.
J Clin Endocrinol Metab. 2008 Jun;93(6):2366-74. doi: 10.1210/jc.2007-2813. Epub 2008 Mar 25.
Experimental and clinical studies in a variety of nonprimate species demonstrate that progesterone withdrawal leads to changes in gene expression that initiate parturition at term. Mice deficient in 5alpha-reductase type I fail to undergo cervical ripening at term despite the timely onset of luteolysis and progesterone withdrawal in blood.
Our objective was to test the hypothesis that estrogen and progesterone metabolism is regulated in cervical tissues during pregnancy, even in species in which parturition is not characterized by progesterone withdrawal in blood.
Estradiol and progesterone metabolism was quantified in intact cervical tissues from nonpregnant and pregnant women at term before or after labor.
The study was conducted at a university hospital.
Tissues were obtained from five nonpregnant and 21 pregnant women (nine before labor and 12 in labor).
Enzyme activity measurements, Northern blot analysis, quantitative real-time RT-PCR, and immunohistochemistry were used to quantify steroid hormone metabolizing enzymes in cervical and myometrial tissues.
During pregnancy, 17beta-hydroxysteroid dehydrogenase type 2 was induced in glandular epithelial cells to catalyze the conversion of estradiol to estrone and stroma-derived 20alpha-hydroxyprogesterone to progesterone. During parturition, 17beta-hydroxysteroid dehydrogenase type 2 was down-regulated in endocervical cells, thereby creating a microenvironment favorable for cervical ripening.
Together, the data indicate that cervical ripening during parturition involves localized regulation of estrogen and progesterone metabolism through a complex relationship between cervical epithelium and stroma, and that steroid hormone metabolism in cervical tissues from pregnant women is unique from that in mice.
对多种非灵长类物种进行的实验和临床研究表明，孕酮撤退会导致基因表达发生变化，从而在足月时启动分娩。I型5α-还原酶缺陷的小鼠尽管黄体溶解及时且血液中孕酮撤退，但足月时仍无法发生宫颈成熟。
我们的目的是检验这样一个假设，即即使在分娩并非以血液中孕酮撤退为特征的物种中，妊娠期间宫颈组织中的雌激素和孕酮代谢也受到调节。
在分娩前后，对足月非妊娠和妊娠妇女完整的宫颈组织中的雌二醇和孕酮代谢进行定量。
该研究在一家大学医院进行。
组织取自5名非妊娠妇女和21名妊娠妇女（9名临产前和12名分娩时）。
采用酶活性测定、Northern印迹分析、定量实时逆转录聚合酶链反应和免疫组织化学方法对宫颈和子宫肌层组织中的甾体激素代谢酶进行定量。
妊娠期间，2型17β-羟基类固醇脱氢酶在腺上皮细胞中被诱导，催化雌二醇转化为雌酮以及基质来源的20α-羟基孕酮转化为孕酮。分娩期间，2型17β-羟基类固醇脱氢酶在内宫颈细胞中下调，从而创造有利于宫颈成熟的微环境。
总之，数据表明分娩期间宫颈成熟涉及宫颈上皮和基质之间复杂关系对雌激素和孕酮代谢的局部调节，并且妊娠妇女宫颈组织中的甾体激素代谢与小鼠不同。
