Release of Porcine Sperm from Oviduct Cells is Stimulated by Progesterone and Requires CatSper
Release of Porcine Sperm from Oviduct Cells is Stimulated by Progesterone and Requires CatSper
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DOI：
10.1038/s41598-019-55834-z
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发表时间：
2019-12-20
影响因子：
4.6
通讯作者：
Miller, David J.
中科院分区：
文献类型：
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作者：
Machado, Sergio A.;Sharif, Momal;Miller, David J.
在交配后和排卵前将精子储存在雌性生殖道中是许多物种使用的生殖策略。当授精和排卵不同步时，功能性精子库的形成和维持提高了受精的可能性。在哺乳动物中，输卵管调节精子功能，如Ca 2+流入和与精子成熟相关的过程，统称为获能。一部分储存的精子通过未知的机制释放出来，并移动到受精部位。输卵管中的激素环境与精子脱离之间存在经验关联;因此，我们直接测试了孕酮诱导精子从输卵管细胞聚集体中释放的能力。精子被允许与输卵管细胞或固定的输卵管聚糖结合，然后用孕酮激发，孕酮刺激48%的精子从输卵管细胞或68%的精子从固定的输卵管聚糖释放。孕酮对精子释放的影响是特异性的;双烯醇酮和17 α-OH-孕酮不影响精子释放。Ca 2+内流进入精子与获能和超活化运动的发展相关。孕酮增加精子细胞内Ca 2+，通过使用NNC 055-0396阻断精子特异性Ca 2+通道CatSper消除。NNC 055-0396还阻断了孕酮诱导的精子从输卵管细胞或固定聚糖中释放。一种激活CatSper的非基因组孕酮受体抑制剂也同样阻止了精子的释放。这是第一份报告表明，从精子库中释放精子是通过CatSper通道的孕酮作用诱导的。
Sperm storage in the female reproductive tract after mating and before ovulation is a reproductive strategy used by many species. When insemination and ovulation are poorly synchronized, the formation and maintenance of a functional sperm reservoir improves the possibility of fertilization. In mammals, the oviduct regulates sperm functions, such as Ca2+ influx and processes associated with sperm maturation, collectively known as capacitation. A fraction of the stored sperm is released by unknown mechanisms and moves to the site of fertilization. There is an empirical association between the hormonal milieu in the oviduct and sperm detachment; therefore, we tested directly the ability of progesterone to induce sperm release from oviduct cell aggregates. Sperm were allowed to bind to oviduct cells or an immobilized oviduct glycan and then challenged with progesterone, which stimulated the release of 48% of sperm from oviduct cells or 68% of sperm from an immobilized oviduct glycan. The effect of progesterone on sperm release was specific; pregnenolone and 17 alpha-OH-progesterone did not affect sperm release. Ca2+ influx into sperm is associated with capacitation and development of hyperactivated motility. Progesterone increased sperm intracellular Ca2+, which was abrogated by blocking the sperm-specific Ca2+ channel CatSper with NNC 055-0396. NNC 055-0396 also blocked the progesterone-induced sperm release from oviduct cells or immobilized glycan. An inhibitor of the non-genomic progesterone receptor that activates CatSper similarly blocked sperm release. This is the first report indicating that release of sperm from the sperm reservoir is induced by progesterone action through CatSper channels.