ESTROGEN REGULATION OF EPIDERMAL GROWTH-FACTOR RECEPTOR MESSENGER RIBONUCLEIC-ACID
ESTROGEN REGULATION OF EPIDERMAL GROWTH-FACTOR RECEPTOR MESSENGER RIBONUCLEIC-ACID
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DOI：
10.1210/mend-2-3-230
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发表时间：
1988-03-01
影响因子：
--
通讯作者：
LOOSEMITCHELL, DS
中科院分区：
文献类型：
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作者：
LINGHAM, RB;STANCEL, GM;LOOSEMITCHELL, DS
先前的研究表明，17β-雌二醇(E_2)可使子宫膜上的表皮生长因子(EGF)受体增加3倍。我们现在报告，子宫EGF受体水平的增加是由于EGF受体mRNA的稳态水平增加。单次注射E2后，EGF受体的mRNA水平在1-3小时内增加3-4倍，在6小时内保持升高，在12-18小时内下降。这种作用是雌二醇所特有的，因为非雌激素激素孕酮、地塞米松、5-α-二氢睾酮和非活性的立体异构体--17-α-雌二醇没有作用。放线菌素D可阻断E2介导的EGF受体基因表达的上调，但嘌呤霉素可阻断该作用。综上所述，这些结果表明，E2通过增加VIV中EGF受体mRNA的稳态浓度来调节EGF受体的水平。
Previous studies have demonstrated that 17.beta.-estradiol (E2) causes a 3-fold increase in epidermal growth factor (EGF) receptors in uterine membranes. We now report that the increase in uterine EGF receptor levels is due to an increase in the steady-state levels of EGF receptor mRNA. After a single E2 injection, EGF receptor mRNA levels, as determined by RNA blots, increase 3- to 4-fold between 1 and 3 h, remain elevated at 6 h, and decline between 12 and 18 h. The effect is specific for E2 since the nonestrogenic hormones progesterone, dexamethasone, 5.alpha.-dihydrotestosterone, and the inactive stereoisomer of E2, 17.alpha.-estradiol, are without effect. E2-Mediated increases in EGF receptor mRNA levels are blocked by actinomycin D but no by puromycin. Taken together, these results indicate tht E2 regulates the level of EGF receptor by increasing the steady-state concentration of EGF receptor mRNA in viv.