Key result
Sperm incubation with MAS agonist Ang-(1-7) activated the PI3K/AKT pathway and improved motility in asthenozoospermic patients (P < 0.01 vs control), an effect blocked by antagonist A779.
Why the study?
The role of the Ang-(1-7)/MAS receptor axis in human sperm function, particularly motility and acrosome reaction, is not well understood.
Does MAS agonist Ang-(1-7) improve sperm motility and acrosome reaction in human spermatozoa?
Does MAS agonist Ang-(1-7) improve sperm motility and acrosome reaction in human spermatozoa?
Answers are grounded in this paper and cite their sources.
The ACE2/Ang-(1-7)/Mas axis improves sperm motility in asthenozoospermic patients in vitro, suggesting a potential biochemical target for male infertility.
Rennin-angiotensin system (RAS) has been involved in sperm function, even so, little is known about the implication of one of the RAS axis formed by Ang-(1-7) (angiotensin-(1-7)) and MAS receptor. Hence, in the present work, we focused on elucidating the function of the MAS receptor in human spermatozoa. We analyzed the expression and localization of MAS receptor in human spermatozoa and we observed if its activation is able to modulate the sperm motility of normal motility and/or asthenozoospermic patients, as well as, the acrosome reaction of the spermatozoa. MAS receptor is present in human mature spermatozoa, not only at the mRNA level but also at protein level. MAS is localized at the acrosome region, as well as, in the tail of spermatozoa. The sperm incubation with MAS agonist Ang-(1-7) activates at dose-dependent manner the PI3K/AKT pathway (P < 0.01 vs control) and improves the motility of asthenozoospermic patients (P < 0.01 vs control), which is blocked by the specific antagonist (A779) (P < 0.01), but it do not modulate the acrosome reaction. These findings suggest that the ACE2/Ang-(1-7)/Mas axis may be a useful biochemical tool for the treatment of male infertility related to sperm mobility.
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Valdivia et al. (2019) studied Asthenozoospermia. MAS agonist Ang-(1-7) vs. Control and specific antagonist (A779) was evaluated on Sperm motility and PI3K/AKT pathway activation (p=<0.01). Sperm incubation with MAS agonist Ang-(1-7) activated the PI3K/AKT pathway and improved motility in asthenozoospermic patients (P < 0.01 vs control), an effect blocked by antagonist A779.
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