Universidad Buenos Aires (UBA), Facultad de Medicina, (CONICET-UBA) Centro de Estudios Farmacológicos y Botánicos (CEFYBO), C1121ABG, Buenos Aires, Argentina.
Department of Pharmacology and Therapeutics, McGill University, Montreal, QC, H3G 1Y6, Canada.
Sci Rep. 2020 Sep 24;10(1):15619. doi: 10.1038/s41598-020-72425-5.
Previously we demonstrated that multidrug resistance-associated protein 4 transporter (MRP4) mediates cAMP efflux in bovine spermatozoa and that extracellular cAMP (ecAMP) triggers events associated to capacitation. Here, we deepen the study of the role of MRP4 in bovine sperm function by using MK571, an MRP4 inhibitor. The incubation of spermatozoa with MK571 during 45 min inhibited capacitation-associated events. MRP4 was localized in post-acrosomal region and mid-piece at 15 min capacitation, while at 45 min it was mainly located in the acrosome. After 15 min, MK571 decreased total sperm motility (TM), progressive motility (PM) and several kinematic parameters. The addition of ecAMP rescued MK571 effect and ecAMP alone increased the percentage of motile sperm and kinematics parameters. Since actin cytoskeleton plays essential roles in the regulation of sperm motility, we investigated if MRP4 activity might affect actin polymerization. After 15 min capacitation, an increase in F-actin was observed, which was inhibited by MK571. This effect was reverted by the addition of ecAMP. Furthermore, ecAMP alone increased F-actin levels while no F-actin was detected with ecAMP in the presence of PKA inhibitors. Our results support the importance of cAMP efflux through MRP4 in sperm capacitation and suggest its involvement in the regulation of actin polymerization and motility.
先前我们证实多药耐药相关蛋白 4 转运体(MRP4)介导牛精子细胞中 cAMP 的外排,且细胞外 cAMP(ecAMP)触发与获能相关的事件。在此,我们通过使用 MRP4 抑制剂 MK571 进一步研究了 MRP4 在牛精子功能中的作用。在 45 分钟的孵育过程中,MK571 抑制了与获能相关的事件。MRP4 在 15 分钟获能时定位于顶体后区和中段,而在 45 分钟时主要位于顶体。15 分钟后,MK571 降低了总精子运动(TM)、前向运动(PM)和几个运动学参数。添加 ecAMP 可挽救 MK571 的作用,而 ecAMP 本身可增加运动精子的百分比和运动学参数。由于肌动蛋白细胞骨架在精子运动的调节中起着重要作用,我们研究了 MRP4 活性是否可能影响肌动蛋白聚合。在 15 分钟获能后,观察到 F-肌动蛋白增加,MK571 抑制了这一增加。这种效应可通过添加 ecAMP 逆转。此外,ecAMP 单独增加 F-肌动蛋白水平,而在 PKA 抑制剂存在下,ecAMP 单独添加时则没有检测到 F-肌动蛋白。我们的结果支持了 cAMP 通过 MRP4 外排在精子获能中的重要性,并表明其参与了肌动蛋白聚合和运动的调节。