Abstract

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Myostatin is a protein secreted by muscle tissue and is an inhibitor of muscle growth. Previous studies have shown that maternal myostatin deficiency during pregnancy increases body mass of wildtype fetuses. This suggests that myostatin-deficient dams can affect the development of their offspring during gestation, but the pathway through which maternal myostatin affects offspring is unknown. Previously, we have shown that maternal myostatin cannot cross the placenta to act directly on the fetus. The placenta could potentially play a role in myostatin-deficient dams by transporting more nutrients to the offspring, resulting in a higher body mass. We hypothesize that myostatin inhibits blood flow into the placenta, thus decreasing nutrient transport. The labyrinth zone of the placenta is responsible for the exchange of nutrients and gases from maternal to fetal blood and the junctional zone is responsible for producing hormones, growth factors and cytokines. Based on our hypothesis, we predict that a dam heterozygous for a myostatin mutation (Mstn/-) mated with a WT male will have placentas with a larger than normal labyrinth zone, resulting in a more efficient exchange of nutrients and gases between the mother and fetus. In this study, we mated reciprocal crosses of WT and myostatin deficient parents. On day 17.5 of gestation, the placentas were collected. The junctional and labyrinth zone, along with maternal and fetal blood spaces within the labyrinth were imaged and their cross-sectional areas were analyzed via ImageJ. The placentas were then analyzed by using PCR for fetal genotype and sex.  There were no statistically significant differences in the labyrinth and junctional zone areas between WT dams and Mstn/- dams.