Kurita T, Young P, Brody J R, Lydon J P, O'Malley B W, Cunha G R
Department of Anatomy, University of California, San Francisco 94143, USA.
Endocrinology. 1998 Nov;139(11):4708-13. doi: 10.1210/endo.139.11.6317.
The role of epithelial and stromal progesterone (P) receptors (PR) in the regulation of uterine epithelial DNA synthesis by P was investigated by analyzing the four types of tissue recombinants prepared with uterine stroma (S) and epithelium (E) from wild-type (wt) and PR knockout (PRKO) mice: wt-S + wt-E, PRKO-S + PRKO-E, wt-S + PRKO-E, and PRKO-S + wt-E. 17-Beta estradiol (E2) stimulated DNA synthesis in all four types of tissue recombinants. On the other hand, P inhibited E2-induced DNA synthesis only in tissue recombinants prepared with wild-type (PR-positive) stroma (wt-S + wt-E or wt-S + PRKO-E) but not knockout (PR-negative) stroma (PRKO-S + wt-E or PRKO-S + PRKO-E). These results clearly demonstrate that the inhibitory effect of P on uterine epithelial DNA synthesis is mediated by stromal PR. Epithelial PR is neither necessary nor sufficient for P inhibition of E2-induced epithelial DNA synthesis.
通过分析用野生型（wt）和孕激素受体基因敲除（PRKO）小鼠的子宫基质（S）和上皮（E）制备的四种类型的组织重组体，研究了上皮和基质孕激素（P）受体（PR）在P调节子宫上皮DNA合成中的作用：wt-S + wt-E、PRKO-S + PRKO-E、wt-S + PRKO-E和PRKO-S + wt-E。17-β雌二醇（E2）刺激了所有四种类型组织重组体中的DNA合成。另一方面，P仅在由野生型（PR阳性）基质制备的组织重组体（wt-S + wt-E或wt-S + PRKO-E）中抑制E2诱导的DNA合成，而在基因敲除（PR阴性）基质（PRKO-S + wt-E或PRKO-S + PRKO-E）中则无此作用。这些结果清楚地表明，P对子宫上皮DNA合成的抑制作用是由基质PR介导的。上皮PR对于P抑制E2诱导的上皮DNA合成既非必需也不充分。
