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In vitro study demonstrates that MRP4 transporter inhibition disrupts cAMP homeostasis and motility in human sperm, indicating its essential role in fertilization.
Cyclic AMP (cAMP) regulates multiple aspects of sperm function essential for attaining fertilizing ability; therefore, its intracellular levels must be tightly controlled to ensure proper signaling dynamics. In recent years, multidrug resistance-associated protein 4 (MRP4) has emerged as a novel regulator of cAMP homeostasis by facilitating its efflux. Previous studies from our laboratory have identified MRP4 in mammalian sperm and demonstrated its role in capacitation-associated events in murine and bovine species. However, its relevance in human sperm remains unknown. Our study demonstrates a functional MRP4 in human sperm, as its pharmacological inhibition led to a rapid (5 min) intracellular cAMP accumulation and a subsequent decrease in extracellular levels (30 min) under capacitating conditions, as assessed by radio binding protein assay. At the biological level, MRP4 inhibition resulted in a decrease in tyrosine phosphorylation at 360 min of capacitation. Membrane hyperpolarization was also affected, diminishing the induced acrosome reaction. Moreover, a significant reduction in intracellular Ca2+ levels was observed, leading to a significant decrease in progressive and total motility, as well as an inhibition of hyperactivation. In addition, our results indicated that the decrease in Ca2+ levels was due to impaired CatSper channel activity upon MRP4 inhibition. These findings suggest that MRP4-mediated cAMP efflux is essential for proper sperm function, playing a critical role in maintaining nucleotide homeostasis, which is a key determinant in the regulation of human sperm capacitation.
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Río et al. (2025) studied this question.
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