AI Article Synopsis
- The study investigates how progestin hormones rapidly stimulate sperm motility in Atlantic croaker fish, focusing on specific signaling pathways.
- Key proteins involved include epidermal growth factor receptors (Egfr and ErbB2) and the mitogen-activated protein kinase (Mapk), which are affected by inhibitors that block sperm hypermotility.
- Results show that activating mPRα (the membrane progestin receptor-alpha) leads to increased sperm motility through the Egfr, ErbB2, and Mapk signaling pathways, highlighting their crucial roles in this process.
Article Abstract
The intracellular pathways mediating rapid, nongenomic progestin stimulation of sperm motility remain unclear. The role of epidermal growth factor receptors (Egfr and ErbB2) and mitogen-activated protein kinase (Mapk) in membrane progestin receptor-alpha (mPRα)-mediated progestin stimulation of sperm hypermotility was examined in a teleost, Atlantic croaker. Inhibition of upstream regulators of Egfr, intracellular tyrosine kinase (Src) with PP2, and matrix metalloproteinase (MMP) with Ilomastat, abolished progestin-initiated sperm hypermotility by 17,20β,21-trihydroxy-4-pregnen-3-one (20β-S; 20 nM) and a specific mPRα agonist, Org OD 02-0 (20 nM). Pretreatment of croaker sperm with EGFR inhibitors, AG1478 (5 μM) and RG13022 (50 μM), the ErbB2 inhibitor, AG879 (5 nM), or the MEK1/2 inhibitor, U0126 (500 nM) blocked progestin stimulation of sperm motility. Levels of phosphorylated extracellular-related kinase 1 and 2 (P-Erk1/2) were increased after 20β-S treatment. These results demonstrate that progestin-mediated hypermotility via mPRα in croaker sperm involves activation of the Egfr, ErbB2 and Mapk pathways.
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| http://dx.doi.org/10.1016/j.mce.2015.06.023 | DOI Listing |
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