In Vivo Regulation of Syndecan-3 Expression in the Rat Uterus by 17β-Estradiol*
In Vivo Regulation of Syndecan-3 Expression in the Rat Uterus by 17β-Estradiol*
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DOI：
10.1074/jbc.m004106200
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发表时间：
2001-01
期刊：
影响因子：
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通讯作者：
L. Russo;S. Calabro;T. A. Filler;D. Carey;R. Gardner
中科院分区：
文献类型：
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作者：
L. Russo;S. Calabro;T. A. Filler;D. Carey;R. Gardner
未成熟大鼠子宫已被广泛用作研究类固醇激素作用的分子机制的体内模型系统。在这项研究中，我们证明了类固醇激素17β-雌二醇对大鼠子宫syndecan-3表达的调节作用。对切除卵巢的未成熟动物给予单次生理剂量的17β-雌二醇（40 μg/kg）可诱导子宫syndecan-3 mRNA的快速和短暂增加。激素给药后4小时，转录水平达到3倍以上的盐水对照组织的峰值升高。放线菌素D而不是放线菌酮对信息上调的抑制表明激素反应依赖于RNA转录而不是新蛋白质合成。雌激素配体雌三醇和他莫昔芬也能有效提高syndecan-3 mRNA水平;然而，非雌激素配体，包括孕酮、5α-二氢睾酮和地塞米松，未能刺激mRNA水平的变化。激素诱导的mRNA的变化导致syndecan-3蛋白含量的短暂变化和子宫内膜上皮细胞时空表达的显著改变。总的来说，这些数据表明类固醇激素17β-雌二醇通过雌激素受体依赖性机制调节子宫中syndecan-3基因的转录。这种雌激素调节的syndecan-3的表达可能在组织超微结构的变化中发挥重要作用，这些变化对子宫正常生长至关重要。
The immature rat uterus has been extensively used as an in vivo model system to study the molecular mechanisms of steroid hormone actions. In this study, we demonstrated the regulated expression of syndecan-3 in the rat uterus by the steroid hormone 17β-estradiol. Administration of a single physiological dose of 17β-estradiol (40 μg/kg) to ovariectomized immature animals induced a rapid and transient increase in uterine syndecan-3 mRNA. Transcript levels reached a peak elevation of 3-fold above saline control tissues 4 h after hormone administration. Inhibition of message up-regulation by actinomycin D but not cycloheximide indicated a hormone response dependent on RNA transcription but not new protein synthesis. The estrogenic ligands estriol and tamoxifen were also effective at raising syndecan-3 mRNA levels; however, nonestrogenic ligands, including progesterone, 5α-dihydrotestosterone, and dexamethasone, failed to stimulate a change in mRNA levels. Hormone-induced changes in mRNA led to transient changes in syndecan-3 protein content and significant alteration in the temporal and spatial expression in endometrial epithelial cells. Collectively, these data show that the steroid hormone 17β-estradiol, regulates transcription of the syndecan-3 gene in the uterus via an estrogen receptor-dependent mechanism. This estrogen-regulated expression of syndecan-3 may play an important role in changes in tissue ultrastructure crucial for proper uterine growth.