Takeyama J, Sasano H, Suzuki T, Iinuma K, Nagura H, Andersson S
Department of Pathology, Tohoku University School of Medicine, Sendai, Japan.
J Clin Endocrinol Metab. 1998 Oct;83(10):3710-5. doi: 10.1210/jcem.83.10.5212.
In estrogen metabolism, the enzymatic properties of the 17beta-hydroxysteroid dehydrogenase (17betaHSD) isozymes play very important roles in steroid hormone metabolism in various tissues, including the placenta. 17betaHSD type 1 catalyzes primarily the reduction of estrone (E1) to estradiol (E2), whereas 17betaHSD type 2 catalyzes primarily the oxidation of E2 to E1. In this study, we examined immunohistochemical localization of 17betaHSD types 1 and 2 in human placenta (31 cases) ranging from 4-40 weeks gestation. The immunoreactivity of 17betaHSD type 1 was exclusively detected in syncytiotrophoblast from 4 weeks gestation to term placenta. Immunoreactivity of 17betaHSD type 2 first appeared in endothelial cells of intravillous vessels at 12 weeks gestation, and the number of 17betaHSD type 2-positive endothelial cells markedly increased up to 19 weeks, then reached a plateau. We quantitatively evaluated the 17betaHSD type 2-positive endothelial cells in chorionic villi and determined the ratio of 17betaHSD type 2-positive endothelial cells using immunohistochemistry of CD34, an endothelial antigen, in serial mirror tissue sections and subsequent image analysis using CAS 200. CD34 was detected from 4 weeks gestation, and its positive areas continued to increase toward term. The 17betaHSD type 2-positive area per CD34-positive area markedly increased from 13 weeks gestation and reached a plateau at 19 weeks gestation, in which almost all endothelial cells were positive for 17betaHSD type 2. 17BetaHSD type 2, therefore, is considered to prevent the passage of excessive estrogens into the fetal circulation at endothelial cells of the intravillous fetal capillaries by catalyzing the inactivation ofE2 to E1.
在雌激素代谢过程中，17β - 羟基类固醇脱氢酶（17βHSD）同工酶的酶学特性在包括胎盘在内的各种组织的类固醇激素代谢中发挥着非常重要的作用。1型17βHSD主要催化雌酮（E1）还原为雌二醇（E2），而2型17βHSD主要催化E2氧化为E1。在本研究中，我们检测了1型和2型17βHSD在妊娠4至40周的人胎盘（31例）中的免疫组织化学定位。1型17βHSD的免疫反应性仅在妊娠4周的合体滋养层细胞直至足月胎盘中检测到。2型17βHSD的免疫反应性在妊娠12周时首次出现在绒毛内血管的内皮细胞中，2型17βHSD阳性内皮细胞的数量在19周时显著增加，然后达到稳定水平。我们在绒毛膜绒毛中对2型17βHSD阳性内皮细胞进行了定量评估，并使用内皮抗原CD34的免疫组织化学方法，在连续的镜像组织切片中确定了2型17βHSD阳性内皮细胞的比例，随后使用CAS 200进行图像分析。CD34在妊娠4周时即可检测到，其阳性区域持续增加直至足月。每CD34阳性区域的2型17βHSD阳性区域从妊娠13周开始显著增加，并在妊娠19周时达到稳定水平，此时几乎所有内皮细胞均为2型17βHSD阳性。因此，2型17βHSD被认为通过催化E2失活为E1，在绒毛内胎儿毛细血管的内皮细胞处防止过量雌激素进入胎儿循环。
