Jirkovská Marie, Kučera Tomáš, Dvořáková Veronika, Jadrníček Martin, Moravcová Milena, Žižka Zdeněk, Krejčí Vratislav
Institute of Histology and Embryology, First Faculty of Medicine, Charles University in Prague, Albertov 4, CZ-128 01 Prague 2, Czech Republic.
Institute of Histology and Embryology, First Faculty of Medicine, Charles University in Prague, Albertov 4, CZ-128 01 Prague 2, Czech Republic.
Placenta. 2016 Apr;40:1-7. doi: 10.1016/j.placenta.2016.02.003. Epub 2016 Feb 9.
Maternal diabetes mellitus changes morphology and impairs function of placental capillaries. Here, quantitative parameters characterizing cell proliferation using detection of Ki67, differentiation reflected by nestin expression and apoptosis in placental capillary bed with active caspase 3 as a marker were compared in normal term placentas and placentas from pregnancies complicated by Type 1 maternal diabetes mellitus.
Specimens of sixteen diabetic placentas and eight control placentas were collected by systematic uniform random sampling. Immunohistochemical detections of Ki67, nestin, and active caspase 3 were performed in histological sections of five haphazardly chosen blocks per placenta. Twenty fields of view per section, i.e. one hundred fields of view per placenta, were used for analysis of proliferation as well as of apoptosis, and in approximately 70 capillary cross-sections per placenta the nestin-positive segments of their circumference were measured.
The percentage of Ki67-positive cells counted in the capillary wall was significantly lower in diabetic group. The counts of Ki67-labelled nuclei per villous area unit were significantly lower in cytotrophoblast and capillary wall of terminal villi in diabetic placenta. The proportion of nestin-labeled segments of capillary circumference was significantly higher in placentas of diabetic group. No differences in the numbers of apoptotic cells were found between studied groups.
The results show that the term placenta in Type 1 diabetes has lower potential to enlarge the surface area of structures involved in maternofetal transport, and that the villous capillary bed displays delayed differentiation. Those factors may participate in decreased ability of diabetic placenta to comply with fetal requirements in the final stage of pregnancy.
妊娠糖尿病会改变胎盘毛细血管的形态并损害其功能。在此，我们比较了正常足月胎盘以及患有1型妊娠糖尿病孕妇的胎盘，通过检测Ki67来表征细胞增殖、以巢蛋白表达反映分化情况以及以活化的半胱天冬酶3作为标志物来检测胎盘毛细血管床中的细胞凋亡的定量参数。
通过系统均匀随机抽样收集了16份糖尿病胎盘和8份对照胎盘的样本。对每个胎盘随机选取的5个组织块的组织切片进行Ki67、巢蛋白和活化半胱天冬酶3的免疫组织化学检测。每个切片20个视野，即每个胎盘100个视野，用于分析增殖和凋亡情况，并在每个胎盘大约70个毛细血管横切面中测量其巢蛋白阳性的圆周段。
糖尿病组中毛细血管壁上Ki67阳性细胞的百分比显著降低。糖尿病胎盘的细胞滋养层和终末绒毛毛细血管壁中每绒毛面积单位的Ki67标记核计数显著降低。糖尿病组胎盘的毛细血管圆周巢蛋白标记段的比例显著更高。研究组之间凋亡细胞数量没有差异。
结果表明，1型糖尿病患者足月胎盘扩大母胎转运相关结构表面积的潜力较低，并且绒毛毛细血管床显示出分化延迟。这些因素可能参与了糖尿病胎盘在妊娠末期满足胎儿需求能力的下降。
