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首页> 外文期刊>Journal of Cellular Physiology >Alterations in mammary gland development following neonatal exposure to estradiol, transforming growth factor alpha, and estrogen receptor antagonist ICI 182,780.
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Alterations in mammary gland development following neonatal exposure to estradiol, transforming growth factor alpha, and estrogen receptor antagonist ICI 182,780.

机译：改变在乳腺发展新生儿接触雌二醇,转变生长因子α和雌激素受体

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High fetal/early postnatal levels of estrogen increase breast cancer risk, but the mechanisms remain unknown. Growth factors, such as transforming growth factor alpha (TGF alpha), may participate as secondary modifiers in this process. We characterized a modulatory role of early postnatal exposure to 17 beta-estradiol (E2) on the developing mammary gland morphology by treating intact female CD-1 mice with physiological doses of E2 (2-4 micrograms), human recombinant TGF alpha (4 micrograms), or an estrogen receptor (ER) antagonist ICI 182,780 (20 micrograms) during postnatal days 1-3. Early postnatal exposure of E2 stimulated mammary ductal growth by days 25 and 35, but by day 50 this was inhibited. The level of differentiation from terminal end buds (TEBs) to the lobulo-alveolar units (LAUs) also was reduced by day 50. The number of TEBs was increased throughout most of the development in the female mice exposed to E2 during early life. An exposure to TGF alpha or ICI 182,780 between postnatal days 1 and 3 stimulated ductal growth, formation of TEBs, and the differentiation of mammary epithelial structures. ICI 182,80 treatment also caused hyperplastic lobular-like structures in 54-day-old females. Thus, neonatal exposure to TGF alpha and ICI 182,780 induced both similar (increase in TEBs) and different (increase/decrease in lobulo-alveolar differentiation) developmental changes in the mouse mammary gland, when compared with an exposure to E2. A unique feature of the postnatal E2 treatment was that it inhibited ductal migration by days 50-54. Our data suggest than an exposure to E2 on postnatal days 1-3, possibly combined with secondary epigenetic alterations, leads to various changes within the developing mammary tree. These changes may be potential prerequisites for mammary tumorigenesis.
机译：高胎儿/早期产后雌激素的水平增加患乳腺癌的风险,但机制仍然未知。转化生长因子α(TGFα),可能作为二次参加修饰符的过程。产后早期暴露于17 beta雌二醇(E2)乳腺形态发展把完整的女性cd -老鼠生理剂量的E2(2 - 4微克),人类重组转化生长因子α(4微克),或一个雌激素受体(ER)拮抗剂ICI 182780 (20在产后几天1 - 3微克)。产后的E2刺激乳房导管增长天25 - 35岁,但白天50这是抑制。从终端芽(teb)lobulo-alveolar单位(lau)也减少了50天。在大多数的女性的发展小鼠暴露于E2在早期的生活。产后之间转化生长因子α或ICI 182780天1和3导管刺激增长,形成teb,乳腺的分化上皮结构。增生性lobular-like结构引起的54-day-old女性。转化生长因子α和ICI 182780诱导相似增加(teb)和不同(增加/减少lobulo-alveolar分化)的发展变化小鼠乳腺,相比E2。E2治疗抑制导管由50 - 54天迁移。暴露在E2在产后1 - 3天,可能结合二级表观遗传改变,在发展中会导致不同的变化乳腺树。乳腺肿瘤发生的先决条件。

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