Cell cycle inhibitor p57 expression in normal and diabetic rat placentas during some stages of pregnancy

Placentomegaly, an abnormal increase in the size of the placenta, is commonly seen in human diabetic pregnancies and diabetic animal experimental models. Proper placental development depends on the proliferation and differentiation of trophoblasts. However, our knowledge about the mitotic regulators that play key roles in synchronizing these events is limited. p57 is a cyclin-dependent kinase (CDK) inhibitor acting in the G1/S transition of the cell cycle. There is no data regarding p57 expression in either rat or human diabetic placentas. The purpose of this study was to investigate p57 expression in control and diabetic rat placentas at different stages of pregnancy. Diabetes was induced by streptozotocin on the first day of pregnancy, and placentas were taken on days 11, 13, 17, and 21 of pregnancy. Our results showed that on day 11, p57 immunostaining intensity was stronger in control group placentas compared to the diabetic group. On day 13, p57 immunostaining intensity increased in both groups, but increased more in the diabetic group. On day 17, p57 immunostaining intensity decreased in both the control and diabetic groups compared to day 13, yet the intensity remained higher in control placentas compared to diabetic placentas. On day 21 of pregnancy, p57 immunostaining intensity increased in the control group and it decreased from the day 17 level in the diabetic group. Western blot results showed consistency with immunohistochemistry results. Our study shows different expression patterns of p57 between control and diabetic rat placentas, which indicate p57 may play a role in abnormal placental formation resulting in placentomegaly arising from diabetes.