Estrogen and luminal stimulation of rat uterine kallikrein
Estrogen and luminal stimulation of rat uterine kallikrein
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雌激素和腔内刺激大鼠子宫泌乳素
DOI：
10.1095/biolreprod56.6.1432
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发表时间：
1997-06-01
影响因子：
3.6
通讯作者：
Valdes, G
中科院分区：
文献类型：
--
作者：
Corthorn, J;Figueroa, C;Valdes, G
为了了解大鼠子宫激肽释放酶的调节，我们评估了其在卵巢切除并补充雌二醇或孕酮的动物中的变化，在腔内油刺激或未刺激的假孕动物中，以及在单侧妊娠动物中的变化。通过对rK 1（真组织激肽释放酶）高度特异性的RIA测定，在补充雌二醇的卵巢切除大鼠中，激肽释放酶的含量升高（0.28 +/- 0.03至0.44 +/- 0.05 ng/mg），而在补充孕酮的情况下降低（0.13 +/- 0.02 ng/mg; n = 15; p < 0.001）。激肽释放酶含量从假孕激素（PP 1）的第1天上升到PP 7的最大值（0.18 +/- 0.01至0.39 +/- 0.04 ng/mg蛋白; n = 36; p < 0.001）。在单侧油腔内刺激的PP 7上，蜕膜化角的激肽释放酶含量高于对侧（0.98 +/- 0.09 vs. 0.35 +/- 0.05 ng/mg蛋白; n = 7; p < 0.001）。免疫细胞化学显示rK 1主要定位于腔上皮和腺上皮，在刺激的角增加。在单侧妊娠大鼠第7天，受精角的激肽释放酶含量高于对侧对照（0.71 +/- 0.07 vs. 0.37 +/- 0.03 ng/mg蛋白，pt 0.001; n = 8），以及较高的激肽原酶活性（每角239 +/- 34.3 vs. 83.5 +/- 7.9 ng缓激肽（BK）/h，p < 0.003;每克组织945 +/- 90 vs. 585 +/- 40 ng 8 K/h，p < 0.002; n = 6）。这些结果表明，雌激素刺激，而孕激素抑制，激肽释放酶的生产，和激素调节被覆盖的腔内刺激，从而关联的酶与蜕膜化。
To understand the regulation of rat uterine kallikrein, we evaluated its variations in animals that had been ovariectomized and supplemented with estradiol or progesterone, in pseudopregnant animals intraluminally oil-stimulated or unstimulated, and in unilaterally pregnant animals. The content of kallikrein, determined by an RIA highly specific for rK1 (true tissue kallikrein), rose in ovariectomized rats with estradiol supplementation (0.28 +/- 0.03 to 0.44 +/- 0.05 ng/mg) and decreased with progesterone (0.13 +/- 0.02 ng/mg; n = 15; p < 0.001). Kallikrein content rose from Day 1 of pseudopregnancy (PP1) to a maximum on PP7 (0.18 +/- 0.01 to 0.39 +/- 0.04 ng/mg protein; n = 36; p < 0.001). On PP7 with unilateral oil intraluminal stimulation, the decidualized horn had higher kallikrein content than did the contralateral (0.98 +/- 0.09 vs. 0.35 +/- 0.05 ng/mg protein; n = 7; p < 0.001). Immunocytochemistry revealed that mainly rK1 is localized in the luminal and glandular epithelium, and it increased in the stimulated horn. In the unilaterally pregnant rat on Day 7, the fertile horn had a higher kallikrein content than its contralateral control (0.71 +/- 0.07 vs. 0.37 +/- 0.03 ng/mg protein, pt 0.001; n = 8), as well as a higher kininogenase activity (239 +/- 34.3 vs. 83.5 +/- 7.9 ng bradykinin(BK)/h per horn, p < 0.003; and 945 +/- 90 vs. 585 +/- 40 ng 8K/h per gram tissue, p < 0.002; n = 6). These results indicate that estrogen stimulates, whereas progesterone inhibits, kallikrein production, and that hormonal regulation is overridden by intraluminal stimulation, thus associating the enzyme with decidualization.