Abstract
Arachidonic acid (AA), a compound secreted by Sertoli cells (SC) in a FSH-dependent manner, is able to induce the release of Ca2+ from internal stores in round spermatids and pachytene spermatocytes. In this study, the possible site(s) of action of AA in round spermatids, the signalling pathways associated and the intracellular Ca2+ stores targeted by AA-induced signalling were pharmacologically characterized by measuring intracellular Ca2+ using fluorescent Ca2+ probes. Our results suggest that AA acts by interacting with a fatty acid G protein coupled receptor, initiating a G protein signalling cascade that may involve PLA2 and ERK activation, which in turn opens intracellular ryanodine-sensitive channels as well as NAADP-sensitive channels in acidic intracellular Ca2+ stores. The results presented here also suggest that AMPK and PKA modulate this AA-induced Ca2+ release from intracellular Ca2+ stores in round spermatids. We propose that unsaturated free fatty acid lipid signalling in the seminiferous tubule is a novel regulatory component of rat spermatogenesis.
Highlights
The functional relationship between germ and Sertoli cells (SCs) in the mammalian seminiferous tubules takes place through adhesion molecules and molecules secreted to the extracellular space in the adluminal compartment [1,2,3]
We showed that arachidonic acid (AA) and other unsaturated fatty acids (UFA) were able to release Ca2+ from intracellular Ca2+ stores (ICaS) in a dose-dependent manner in pachytene spermatocytes and round spermatids [11]
GPR120 agonist 3 at 5 and 10 μM, not reaching saturation, was able to induce Ca2+ release from ICaS at higher rates compared to GPR40 agonists, but at lower rates compared to GA or AA at similar concentrations
Summary
The functional relationship between germ and Sertoli cells (SCs) in the mammalian seminiferous tubules takes place through adhesion molecules and molecules secreted to the extracellular space in the adluminal compartment [1,2,3]. We provide evidence that agonists for GPR120 but not for GPR40 (both GPRs activated by medium and long chain FAs) were able to induce an increase in intracellular Ca2+ concentration ([Ca2+]i) in spermatogenic cells in the nominal absence of external Ca2+. This Ca2+ was released from ICaS, to the effects of AA. We provide evidences to support the hypothesis that UFAs can be part of the cell-cell signalling mechanisms in seminiferous tubules, leading to the control of spermatogenic cell differentiation or death by SCs in the testes
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