Department of Histology and Embryology, Faculty of Medicine, Akdeniz University, Antalya, Turkey.
Histol Histopathol. 2012 Jan;27(1):59-68. doi: 10.14670/HH-27.59.
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.
胎盘肿大，即胎盘大小的异常增加，在人类糖尿病妊娠和糖尿病动物实验模型中较为常见。适当的胎盘发育取决于滋养细胞的增殖和分化。然而，我们对于在这些事件中起关键作用的有丝分裂调节剂的了解是有限的。p57 是一种细胞周期蛋白依赖性激酶（CDK）抑制剂，作用于细胞周期的 G1/S 转换期。目前还没有关于 p57 在大鼠或人类糖尿病胎盘中表达的数据。本研究旨在研究不同妊娠阶段的对照组和糖尿病大鼠胎盘中 p57 的表达情况。糖尿病是在妊娠第一天用链脲佐菌素诱导的，在妊娠第 11、13、17 和 21 天取胎盘。我们的结果表明，在第 11 天，对照组胎盘的 p57 免疫染色强度强于糖尿病组。第 13 天，两组的 p57 免疫染色强度均增加，但糖尿病组增加更多。第 17 天，与第 13 天相比，两组的 p57 免疫染色强度均下降，但对照组胎盘的强度仍高于糖尿病组。在妊娠第 21 天，对照组的 p57 免疫染色强度增加，而糖尿病组则从第 17 天的水平下降。Western blot 结果与免疫组织化学结果一致。我们的研究表明，对照组和糖尿病大鼠胎盘中 p57 的表达模式不同，这表明 p57 可能在由糖尿病引起的胎盘肿大的异常胎盘形成中发挥作用。
