Meeting Abstract
In mammals, progesterone production by the corpus luteum (CL) in the ovary is necessary for maintenance of early pregnancy. Chronic stress inhibits progesterone production, and thus results in pregnancy loss in rodents. This effect can be rescued by progesterone supplementation. While substantial research has focused on the downstream mechanisms by which low progesterone contributes to pregnancy loss, the stress-induced changes in receptor signaling and steroidogenic gene expression in the ovary that drive low progesterone production are not well understood. We used a rodent model to investigate proximate mechanisms in the ovary that cause low progesterone production during early pregnancy in response to chronic stress. Female mice were mated and randomly placed in stress or control groups. Stressed animals were restrained for four hours per day for four days following mating. Tissue and plasma samples were collected 5.5 days after mating. On day 5.5 of pregnancy, stressed animals had significantly lower plasma progesterone than control females (P < 0.01). Expression of the long-form prolactin receptor in the ovaries was lower in stressed females (P < 0.05) and was significantly correlated with the expression of steroidogenic enzymes StAR (steroidogenic acute regulatory protein) and P450scc (cholesterol side-chain cleavage enzyme). There was no difference in expression of the S2 or S3 prolactin receptor genes or luteinizing hormone receptor between groups (P > 0.10). Our data indicate that stress disrupts several components of the ovarian steroidogenic pathway, possibly via altered expression of the long-form prolactin receptor in the ovary. Ongoing work will test whether these changes in ovarian gene expression during pregnancy persist throughout gestation and impact overall fecundity.
