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Angiotensin-converting enzyme and male fertility
J R Hagaman1, J S Moyer, E S Bachman
1Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599-7525, USA. hage@med.unc.edu
Summary
Angiotensin-converting enzyme (ACE) is crucial for male fertility in mice. Sperm from mice lacking ACE show impaired oviduct transport and zona pellucida binding, leading to reduced fertilization success.
Area of Science:
- Reproductive Biology
- Enzymology
- Genetics
Background:
- The angiotensin-converting enzyme (ACE) gene encodes somatic and testis-specific isozymes.
- Previous studies showed male mice lacking both ACE isozymes have reduced fertility.
Purpose of the Study:
- To investigate the cause of the male fertility defect in mice lacking both ACE isozymes.
- To determine the specific roles of somatic and testis ACE in male fertility.
Main Methods:
- Gene targeting was used to create mice lacking both ACE isozymes.
- Fertility was assessed, and sperm function (transport and binding) was analyzed in vivo and in vitro.
- Mice lacking only somatic ACE or angiotensinogen were also studied.
Main Results:
- Mice lacking both ACE isozymes exhibited impaired sperm transport in oviducts and reduced binding to zonae pellucidae, resulting in lower in vivo fertilization rates.
- Males lacking only somatic ACE were fertile, indicating testis ACE is sufficient for male fertility.
- Mice lacking angiotensinogen had normal fertility, suggesting angiotensin I is not essential for testis ACE function.
Conclusions:
- Somatic ACE is not essential for male fertility.
- Testis ACE plays a critical role in sperm function, including oviductal transport and zona pellucida binding, which are vital for successful in vivo fertilization.
- Targeting ACE isozymes offers insights into male reproductive mechanisms.