Transient receptor potential-canonical 3 modulates sperm motility and capacitation-associated protein tyrosine phosphorylation via [Ca2+]i mobilization.

Abstract

Ca(2+) signaling is pivotal for sperm maturation, including the processes of motility, capacitation, and the acrosome reaction. As a Ca(2+) conductor, transient receptor potential-canonical 3 (TRPC3) plays an important role in somatic cells. However, the function of TRPC3 in sperm is not well understood. Here, a pharmacological approach was used to investigate the role and mechanism of TPRC3 in sperm function. The TRPC3 antagonist Pyr3 could inhibit sperm motility and accelerate capacitation-associated protein tyrosine phosphorylation in a time- and dose-dependent manner, regardless of the presence or absence of Ca(2+) in the incubation medium. Further investigation revealed that sperm [Ca(2+)]i fell immediately once Pyr3 was added to Ca(2+)-free medium, and then gradually increased and returned to baseline levels. Moreover, the [Ca(2+)]i levels markedly elevated when sperm were incubated for 30 min in the presence of Pyr3; this change was subsequently accompanied by a significant reduction in sperm mitochondrial membrane potential. This study suggested that TRPC3 can modulate sperm function via mobilization of sperm [Ca(2+)]i.