Abstract
Animals deficient in Heme oxygenase-1 (HO-1, Hmox1(-/-) mice) have impaired pregnancies, characterized by intrauterine fetal death. HO-1 expression has been shown to be essential for pregnancy by dictating placentation and intrauterine fetal development. Its absence leads to intrauterine fetal growth restriction and fetal loss, which is independent of the immune system. Defect in previous steps, e.g., ovulation, may, however, also count for their poor reproductive outcome. Here, we investigated ovulation after hormonal hyperstimulation in Hmox1 wild-type and knockout animals. We observed that animals lacking HO-1 produced significantly less oocytes after hormonal stimulation than wild type animals and this was mirrored by the number of corpora lutea in the ovary. Furthermore, ovulated oocytes from Hmox1(-/-) animals were poorly fertilized compared with those from wild-type animals. In conclusion, we demonstrate here that HO-1 plays a pivotal role in the process of oocyte ovulation as well as fertilization, bringing to light a new and unsuspected role for HO-1.
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