Dept. of Medical Science/석사Prenatal stress is known to cause intrauterine growth retardation of fetus and is also associated with various metabolic and neurodevelopmental diseases in adult offspring as long-term effects. In addition, many of the diseases associated with prenatal stress exhibit a sex bias. Perturbations and vulnerability to prenatal stress are often more profound for the male, however, the mechanisms responsible for this relationship are not clear. It was previously shown that administration of dexamethasone at days 7.5, 8.5 and 9.5 post coitum (p.c.), a critical time point in early placenta development, induces placental defects as well as embryonic growth restriction. In this study, we examined the effect of maternal dexamethasone on male testis development as well as on the sex-specific changes in embryonic and placental growth. The prenatal administration of dexamethasone at the same time point led to growth restriction in both females and males at day 11.5 p.c. Afterward, females, but not males, showed restoration to near normal levels at day 18.5 p.c. During the testis development, sex-determining genes (Sry, Sox9, and other downstream genes) were dysregulated by prenatal dexamethasone. Moreover, prenatal exposure to dexamethasone disrupted testosterone level in males. Taken together, this data provides a valuable resource for finding possible mechanisms that cause sex-specific effects in response to prenatal stress.prohibitio
