PROGESTERONE EFFECTS ON DEOXYRIBONUCLEIC-ACID SYNTHESIS IN NORMAL MOUSE MAMMARY-GLANDS
PROGESTERONE EFFECTS ON DEOXYRIBONUCLEIC-ACID SYNTHESIS IN NORMAL MOUSE MAMMARY-GLANDS
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DOI：
10.1210/endo-122-2-464
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发表时间：
1988-02-01
期刊：
影响因子：
4.8
通讯作者：
HASLAM, SZ
中科院分区：
文献类型：
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作者：
HASLAM, SZ
目前的体内和体外数据表明，孕酮 (P) 是成年小鼠乳腺上皮增殖所必需的。 P receptors (PgR) in adult mammary glands are under estrogenic regulation.相比之下，在未成熟的青春期 5 周龄小鼠中，PgR 仅以低浓度存在，并且不能通过雌激素 (E) 增加。确定了具有不同 PgR 组成的两种不同乳腺发育状态后，本研究的目的是研究 E 依赖性和非依赖性 PgR 在上皮细胞增殖中的作用。 DNA 组织放射自显影用于定量 P 对 DNA 合成的影响；还评估了激素对乳腺形态的影响。 The results demonstrate the P, rather than E, has a major role in stimulating epithelial DNA synthesis in the adult mammary gland. P'对细胞增殖的刺激作用的形态学相关性是导管侧分支的增加。我们假设 P 通过 E 依赖性 PgR 发挥作用，并且 E 促进成体组织中上皮细胞增殖的一种重要方式是通过其增加 PgR 浓度的能力。在未成熟的乳腺中，E 而不是 P 在这个发育阶段主要负责刺激上皮细胞增殖。缺乏主要的 P 介导的细胞增殖效应似乎与 E 依赖性 PgR 的缺乏有关。
Current in vivo and in vitro data indicate that progesterone (P) is required for epithelial proliferation in mammary glands of adult mice. P receptors (PgR) in adult mammary glands are under estrogenic regulation. By contrast in immature, pubertal 5-week-old mice, PgR are present only in low concentration and cannot be increased by estrogen (E). Having identified two different mammary gland developmental states with differing PgR compositions, the purpose of the present studies was to investigate the roles of E-dependent and -independent PgR in epithelial cell proliferation. DNA histoautoradiography was used to quantitate the effect of P on DNA synthesis; hormonal effects on mammary gland morphology were also assessed. The results demonstrate the P, rather than E, has a major role in stimulating epithelial DNA synthesis in the adult mammary gland. The morphological correlate of P''s stimulatory effect on cell proliferation was increased ductal side-branching. We postulate that P is acting via E-dependent PgR and that one important way in which E promotes epithelial cell proliferation in adult tissue is by its ability to increase PgR concentration. In the immature mammary gland E rather than P is primarily responsible for stimulation of epithelial cell proliferation at this developmental stage. It appears likely that the absence of a predominant, P-mediated cell proliferative effect is related to the lack of E-dependent PgR.