Temporal relationship between proliferating and apoptotic hormone-producing and endothelial cells in the equine corpus luteum
Temporal relationship between proliferating and apoptotic hormone-producing and endothelial cells in the equine corpus luteum
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DOI：
10.1530/rep.1.01051
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发表时间：
2006-07-01
期刊：
影响因子：
3.8
通讯作者：
Watson, E. D.
中科院分区：
文献类型：
--
作者：
Aguilar, J.;Fraser, H. M.;Watson, E. D.
血管内皮细胞死亡、血管退化和母马激素产生细胞死亡之间的时间关系尚未建立。为了解黄体发育过程中细胞增殖和死亡的动态变化，研究了黄体早、中、晚期和黄体中期用氯前列烯醇处理后黄体过早溶解的情况。用特异性标记物(分别是磷酸化的组蛋白-3和活化的caspase-3)研究细胞增殖和凋亡的变化。组蛋白-3阳性细胞在黄体早期最为丰富，主要存在于内皮细胞。氯前列烯醇处理36h后，激素分泌细胞中组蛋白-3活性显著升高。激活caspase-3染色的频率在第14天达到高峰，并在黄体中期给药36h后被诱导。然而，细胞死亡同时发生在内皮细胞和激素产生细胞中。这些结果表明，一部分激素产生细胞在黄体溶解前后进入细胞分裂的早期阶段，而大多数细胞正在经历细胞死亡。母马自然和诱导的功能性和结构性黄体退化至少部分可以归因于内皮细胞和激素产生细胞的同时凋亡。然而，没有证据表明内皮细胞死亡是自然发生的黄体溶解的触发因素。
The temporal relationship between endothelial cell death, vascular regression and the death of hormone-producing cells in the mare has not been established. To determine the dynamics of cell proliferation and death throughout the luteal phase, corpora lutea were studied at the early, mid- and late luteal phase, and after treatment with cloprostenol in the mid-luteal phase to induce premature luteolysis. Changes in cell proliferation and apoptosis were investigated utilising specific markers (phosphorylated histone-3 and activated caspase-3 respectively). Histone-3 positive cells were most abundant during the early luteal phase, and were mainly present in endothelial cells. Histone-3 activity significantly increased in hormone-producing cells 36 h after cloprostenol treatment. Frequency of activated caspase-3 staining peaked on day 14, and was induced by 36 h after cloprostenol administration in mid-luteal phase. However, cell death occurred simultaneously in the endothelial and hormone-producing cells. These results show that a subset of hormone-producing cells enter the early stages of cell division around luteolysis, while the majority of cells are undergoing cell death. Natural and induced functional and structural luteal regression in the mare can be at least partially attributed to simultaneous apoptosis of endothelial and hormone-producing cells. However, there is no evidence that endothelial cell death is the trigger for naturally occurring luteolysis.