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DOI：
10.1210/jcem.85.1.6229
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发表时间：
2000
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月经后子宫内膜的生长和修复与血管生成密切相关。在这些过程中的异常导致过度或不可预测的出血模式，在许多女性中很常见。因此，了解哪些因素调节正常子宫内膜血管生成是很重要的。血管内皮生长因子（VEGF）是一种内皮细胞特异性的有丝分裂原，在正常和病理性血管生成中起重要作用。在这项研究中，我们表明，VEGF的表达在人子宫内膜缺氧调节。在体外培养24小时，缺氧条件下导致2- 6倍的VEGF分泌增加的基质和上皮细胞分离自人子宫内膜。定量RT-PCR用于测量这些细胞中VEGF信使核糖核酸（mRNA）水平。缺氧后，VEGF mRNA水平在基质细胞中增加1.8倍，在腺上皮细胞中增加3.4倍。每个VEGF剪接变体的mRNA增加到相同的程度。在同一时间用雌二醇或孕酮处理，基质细胞和上皮细胞对缺氧的反应中VEGF分泌的增加没有改变。在月经期间，当类固醇水平较低，但组织是缺血的人子宫内膜原位杂交，表现出强烈的杂交VEGF mRNA在基质和腺细胞。这些结果表明，局部因素，如缺氧，可以调节VEGF在子宫内膜的表达。这可能在月经后子宫内膜的正常修复中起重要作用。在缺氧条件下，子宫内膜细胞分泌的VEGF可能在子宫内膜异位症的发病机制中也很重要，因为当脱落的子宫内膜外植体附着在异位部位时，它可以帮助脱落的子宫内膜外植体进行血管再生。
Endometrial growth and repair after menstruation are associated with profound angiogenesis. Abnormalities in these processes result in excessive or unpredictable bleeding patterns and are common in many women. It is therefore important to understand which factors regulate normal endometrial angiogenesis. Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen that plays an important role in normal and pathological angiogenesis. In this study we show that expression of VEGF is regulated by hypoxia in human endometrium. Culture in vitro for 24 h under hypoxic conditions resulted in a 2- to 6-fold increase in VEGF secretion by both stromal and epithelial cells isolated from human endometrium. Quantitative RT-PCR was used to measure VEGF messenger ribonucleic acid (mRNA) levels in these cells. After hypoxia, VEGF mRNA levels increased 1.8-fold in stromal cells and 3.4-fold in glandular epithelial cells. The mRNA for each VEGF splice variant increased to an equal extent. The increase in VEGF secretion by stromal and epithelial cells in response to hypoxia was not altered by treatment at the same time with estradiol or progesterone. In situ hybridization of human endometrium during menstruation, when steroid levels are low but the tissue is subject to ischemia, showed strong hybridization to VEGF mRNA in both stromal and glandular cells. These results show that local factors, such as hypoxia, can regulate VEGF expression in the endometrium. This may play an important part in normal endometrial repair after menstruation. The secretion of VEGF by endometrial cells under hypoxic conditions may also be important in the pathogenesis of endometriosis, because it would be predicted to assist revascularization of desquamated endometrial explants when they attach at ectopic sites.