Bigsby R M, Cunha G R
Endocrinology. 1985 Dec;117(6):2520-6. doi: 10.1210/endo-117-6-2520.
The effects of progestins and glucocorticoids on cellular proliferation were examined in the uterus of 5-day-old mice by monitoring either the labeling index (LI) after exposure to [methyl-3H]thymidine ([3H]TdR) in vivo or the mitotic index (MI) after colchicine-induced arrest of cells in metaphase. In untreated 5-day-old mice, epithelial LI was 31%, and stromal LI was 15%. Eighteen hours after a single ip injection of 40 mg/kg progesterone, epithelial LI was reduced to 2.3% and remained low for 48 h. Stromal LI increased transiently, reaching a zenith (40%) 18 h after administration of progesterone and returning to control levels by 24 h. When mitotic activity was assessed 24 h after progesterone treatment, epithelial MI was decreased (control, 3.1%; progesterone, 0.23%) and stromal MI was increased (control, 0.60%; progesterone, 2.1%). Thus, the measured effects on LI were indicative of altered proliferative activity of the tissues. Glucocorticoids also inhibited epithelial LI, but had no effect on stromal LI. Eighteen hours after a single ip injection, dexamethasone inhibited epithelial LI to the same extent as progesterone treatment. Corticosterone did not significantly decrease epithelial LI, while cortisol produced an intermediate inhibitory response. To determine whether the high baseline LI in uterine epithelium of neonatal mice was estrogen dependent, uteri of 1-day-old mice were grafted under the kidney capsule of ovariectomized adult mice. Eight days later, the hosts were treated with either progesterone or vehicle and then killed 18 h later. After labeling the tissue with [methyl-3H]thymidine in vitro, the mean LI of the epithelium of the grafted uteri was 11.5%, while that of the vehicle-treated hosts was 0.10%. Progesterone treatment reduced the LI of the grafted uterine epithelium to 1.0%. These data demonstrate that uterine tissues of the neonatal mouse proliferate rapidly in the absence of gonadal steroids. Progestins and glucocorticoids specifically inhibit this estrogen-independent DNA synthesis of uterine epithelium.
通过监测体内暴露于[甲基 - 3H]胸苷（[3H]TdR）后的标记指数（LI）或秋水仙碱诱导细胞停滞在中期后的有丝分裂指数（MI），研究了孕激素和糖皮质激素对5日龄小鼠子宫细胞增殖的影响。在未经处理的5日龄小鼠中，上皮细胞LI为31%，基质LI为15%。单次腹腔注射40mg/kg孕酮18小时后，上皮细胞LI降至2.3%，并在48小时内保持低水平。基质LI短暂增加，在给予孕酮后18小时达到峰值（40%），并在24小时恢复到对照水平。在孕酮处理24小时后评估有丝分裂活性时，上皮细胞MI降低（对照，3.1%；孕酮，0.23%），基质MI增加（对照，0.60%；孕酮，2.1%）。因此，对LI的测量效应表明组织增殖活性发生了改变。糖皮质激素也抑制上皮细胞LI，但对基质LI没有影响。单次腹腔注射18小时后，地塞米松对上皮细胞LI的抑制程度与孕酮处理相同。皮质酮没有显著降低上皮细胞LI，而皮质醇产生了中等程度的抑制反应。为了确定新生小鼠子宫上皮细胞中高基线LI是否依赖雌激素，将1日龄小鼠的子宫移植到去卵巢成年小鼠的肾囊下。8天后，宿主用孕酮或赋形剂处理，然后在18小时后处死。在体外用[甲基 - 3H]胸苷标记组织后，移植子宫上皮细胞的平均LI为11.5%，而用赋形剂处理的宿主为0.10%。孕酮处理将移植子宫上皮细胞的LI降至1.0%。这些数据表明，新生小鼠的子宫组织在没有性腺类固醇的情况下迅速增殖。孕激素和糖皮质激素特异性抑制子宫上皮细胞这种不依赖雌激素的DNA合成。
