Inhibition of early luteal angiogenesis by gonadotropin-releasing hormone antagonist treatment in the primate

Inhibition of early luteal angiogenesis by gonadotropin-releasing hormone antagonist treatment in the primate
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DOI:
10.1210/jc.85.6.2339
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发表时间:
2000-06-01
影响因子:
5.8
通讯作者:
Fraser, HM
Fraser, HM
中科院分区:
医学2区
文献类型:
--
作者:
Dickson, SE;Fraser, HM

文献摘要

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黄体发育过程中的血管生成对于叶黄素细胞的正常功能至关重要,但这一过程的控制以及甾体生成与内皮细胞之间的关系仍有待阐明。本研究的目的是:1)量化绒猴排卵周期黄体期内皮细胞的增殖;2)测定GnRH拮抗剂治疗促性腺激素停药对早期黄体期血管生成高峰的影响;3)描述黄体(CL)的形态学变化。在黄体早期、中期和晚期采集卵巢,通过定量测定溴脱氧尿苷掺入量来测定血管生成活性的变化。在黄体第1天和第2天使用GnRH拮抗剂,第3天收集卵巢。通过计算黄体切片中溴脱氧尿苷免疫阳性细胞的数量,获得增殖指数。细胞增殖在黄体早期最大,在黄体中期和晚期明显下降。GnRH拮抗剂治疗可使早期黄体期增殖峰值降低90%,抑制血浆黄体酮,并严重破坏叶黄素细胞形态。这些结果表明,早期灵长类动物的血管生成依赖于促性腺激素对叶黄素细胞的刺激。
Angiogenesis during luteal development is essential for normal lutein cell function, but the control of this process and the relationships between the steroidogenic and endothelial cells have still to be elucidated. The aim of this study was to: 1) quantify endothelial cell proliferation throughout the luteal phase of the marmoset ovulatory cycle; 2) determine the effect of gonadotropin withdrawal using GnRH antagonist treatment on the early luteal phase angiogenesis peak; and 3) describe the resultant morphological changes in the corpus luteum (CL). Ovaries were collected during the early, mid-, and late luteal phase, and changes in angiogenic activity were determined by quantification of bromodeoxyuridine incorporation. Animals were treated with a GnRH antagonist, on luteal days 1 and 2, and ovaries were collected on day 3. A proliferation index was obtained by counting the number of bromodeoxyuridine immunopositive cells in luteal sections. Cell proliferation was maximal in the early luteal phase and fell significantly in the mid- and late CL. GnRH antagonist treatment reduced the early luteal phase proliferation peak by 90%, suppressed plasma progesterone, and severely disrupted lutein cell morphology. These results demonstrate that the intense angiogenesis in the early primate CL is dependent on gonadotropin stimulation of lutein cells.