Estrogen responses in bovine fetal uterine cells involve pathways directed by both estrogen response element and activator protein-1.
Estrogen responses in bovine fetal uterine cells involve pathways directed by both estrogen response element and activator protein-1.
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牛胎儿子宫细胞中的雌激素反应涉及由雌激素反应元件和激活蛋白-1 共同指导的途径。
DOI：
10.1095/biolreprod60.5.1204
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发表时间：
1999
影响因子：
3.6
通讯作者：
Woods,VM
中科院分区：
文献类型：
--
作者：
Malayer,JR;Cheng,J;Woods,VM
目的是在 ER 类型、增强子类型和配体非依赖性激活的背景下，检查雌激素受体 (ER) 在牛子宫内膜发育中的可能作用。将产生 ERα 或 ERβ 的表达载体导入妊娠第 110 天至 120 天的胎儿子宫细胞（UBF120 细胞）和大鼠胚胎成纤维细胞（Rat-1 细胞）中，这两种细胞都不表达内源 ER。共转染含有雌激素反应元件 (ERE) 或激活蛋白 1 (AP-1) 反应元件的报告构建体。这些报告基因还被转染到妊娠第 180 天至 200 天的胎儿子宫细胞（UBF180 细胞）中，这些细胞表达 ER。在转染 ERα 或 ERβ 的 UBF120 和 Rat-1 细胞中，用 estradiol-17β (E2) 处理导致 ERE 报告构建体活性增加，但 AP-1 元件报告构建体活性增加。抗雌激素 ICI 182,780 (ICI) 对 ERα 和 ERβ 均表现出 E2 拮抗活性。因此，除 ER 外，所有 ERE 的 E2 依赖性转录成分均存在；然而，细胞不具备通过 AP-1 介导的 E2 依赖性转录能力。在 UBF180 细胞中，E2 处理增加了 ERE 和 AP-1 报告基因活性。 ICI表现出E2拮抗剂活性。用表皮生长因子处理导致 ERE 报告基因活性增加，而 ICI 抑制该活性，表明 ER 的配体独立激活。这些数据表明，ER 介导的基因调控的多种途径发生在发育中的胎儿子宫中，并且 ERα 和 ERβ 作用所需的核成分在受体表达之前就存在。
Objectives were to examine possible roles of estrogen receptor (ER) in development of the bovine uterine endometrium in the context of ER type, enhancer type, and ligand-independent activation. Expression vectors producing either ERα or ERβ were introduced into fetal uterine cells from Day 110 to 120 of gestation (UBF120 cells) and into rat embryo fibroblasts (Rat-1 cells), neither of which express endogenous ER. Reporter constructs containing either an estrogen response element (ERE) or activator protein-1 (AP-1) response element were cotransfected. These reporters were also transfected into fetal uterine cells from Day 180 to 200 of gestation (UBF180 cells), which express ER. In UBF120 and Rat-1 cells transfected with either ERα or ERβ, treatment with estradiol-17β (E2) resulted in increased activity of an ERE reporter construct, but not an AP-1 element reporter construct. The antiestrogen ICI 182,780 (ICI) exhibited E2antagonist activity with both ERα and ERβ. Thus, all components were present for E2-dependent transcription from an ERE except ER; however, cells were not competent for E2-dependent transcription mediated through AP-1. In UBF180 cells, E2treatment increased both ERE and AP-1 reporter activity. ICI exhibited E2antagonist activity. Treatment with epidermal growth factor resulted in increased ERE reporter activity that was inhibited by ICI, indicative of ligand-independent activation of ER. These data suggest that multiple pathways for ER-mediated gene regulation occur in the developing fetal uterus and that nuclear components necessary for action of both ERα and ERβ are present prior to expression of the receptor.