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首页> 外文期刊>Molecular reproduction and development >Phosphatidylinositol 3-kinase pathway regulates sperm viability but not capacitation on boar spermatozoa.
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Phosphatidylinositol 3-kinase pathway regulates sperm viability but not capacitation on boar spermatozoa.

机译：磷脂酰肌醇3-激酶途径可调节精子的生存能力，但不能调节公猪精子的获能能力。

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摘要

Phosphatidylinositol 3-kinase (PI3-K) plays an important role in cell survival in somatic cells and recent data pointed out a role for this kinase in sperm capacitation and acrosome reaction (AR). This study was undertaken to evaluate the role of PI3-K pathway on porcine spermatozoa capacitation, AR, and viability using two unrelated PI3-K inhibitors, LY294002 and wortmannin. In boar spermatozoa, we have identified the presence of PDK1, PKB/Akt, and PTEN, three of the main key components of the PI3-K pathway. Incubation of boar sperm in a capacitating medium (TCM) caused a significant increase in the percentage of capacitated (25 +/- 2 to 34 +/- 1% P < 0.05, n = 6) and acrosome reacted (1 +/- 1 to 11 +/- 1% P < 0.01, n = 6) spermatozoa compared with sperm in basal medium (TBM). Inhibition of PI3-K did affect neither the capacitation status nor AR nor protein p32 tyrosine phosphorylation of boar spermatozoa incubated in TBM or TCM. Boar sperm viability in TBM was significantly decreased by 40 and 20% after pretreatment with LY294002 or wortmannin, respectively. Similar results were observed after incubation of boar spermatozoa in TCM. Treatment of boar spermatozoa with the analog of cAMP, 8Br-cAMP significantly prevented the reduction on sperm viability. Our results provide evidence for an important role of the PI3-K pathway in the regulation of boar sperm viability and suggests that other signaling pathways different from PI3-K must be activated downstream of cAMP to contribute to regulation of sperm viability. Finally, in our conditions the PI3-K pathway seems not related with boar sperm capacitation or AR.
机译：磷脂酰肌醇3-激酶（PI3-K）在体细胞的细胞存活中起重要作用，最新数据指出该激酶在精子获能和顶体反应（AR）中的作用。这项研究旨在使用两种不相关的PI3-K抑制剂LY294002和渥曼青霉素评估PI3-K途径在猪精子获能，AR和生存力中的作用。在公猪的精子中，我们确定了PDK1，PKB / Akt和PTEN（PI3-K途径的三个主要关键成分）的存在。将公猪精液孵化在可容性培养基（TCM）中导致可容性（25 +/- 2至34 +/- 1％P <0.05，n = 6）的百分比显着增加，并且顶体反应（1 +/- 1）与基础培养基（TBM）中的精子相比，精子达到11 +/- 1％P <0.01，n = 6）。 PI3-K的抑制作用既不会影响在TBM或TCM中孵育的公猪精子的获能状态，AR或蛋白p32酪氨酸磷酸化。用LY294002或渥曼青霉素预处理后，TBM中的公猪精子活力分别显着降低40％和20％。在中药中孵育公猪精子后，观察到相似的结果。用cAMP，8Br-cAMP类似物处理公猪精子可显着防止精子活力降低。我们的结果提供了PI3-K途径在公猪精子活力调节中的重要作用的证据，并暗示必须在cAMP下游激活不同于PI3-K的其他信号通路，以有助于精子活力的调节。最后，在我们的条件下，PI3-K途径似乎与公猪精子获能或AR无关。

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