Seidmann L, Kamyshanskiy Y, Martin S Z, Fruth A, Roth W
Institute of Pathology, University Medical Centre of the Johannes Gutenberg University, Mainz, Germany.
Institute of Pathology, Karaganda State Medical University, Kazakhstan.
Eur J Obstet Gynecol Reprod Biol. 2017 Aug;215:134-140. doi: 10.1016/j.ejogrb.2017.06.007. Epub 2017 Jun 13.
Villous immaturity for gestational age is a multifactorial developmental deviation associated with unexpected placental insufficiency, fetal hypoxia and term fetal death. In our previous work we have shown that immature CD15+/CD31+/CD34+ endothelial cells were an important indicator of placental villous immaturity and chronic insufficiency. The aim of this study was to perform a comparative analysis of CD15-marked immaturity in the vessel walls between normal and pathological term placentas of clinically and structurally heterogenous groups with normal, low and high weight.
165 clinically normal and pathological placentas of gestational age 39-42 with normal weight (25-75 percentile), low weight (<10 percentile) and high weight (>90 percentile) were structurally and immunohistochemically analyzed. Excluded were placentas with a severe form of placental insufficiency associated with intrauterine fetal death, low APGAR-score, genetic and chromosomal diseases or placental inflammations. The distribution patterns of CD15, CD31 and CD34 were assessed separately in the macrovasculature, microvasculature and placental barrier (PB) - associated capillaries.
All placental groups with normal weight, low weight and high weight include normal, accelerated villous maturation or villous immaturity independent of their weight. However, a significant increase of immature CD15+/CD31+/CD34+ endothelial cells was detected in microvasculature and PB -associated capillaries in high weight-placentas (63.5%/52.2%), compared to those of normal weight (13.8%/8.2%) and low weight (16.1%/17.8%). The distribution of macrovascular immature CD15+/CD31+/CD34+ endothelial cells did not show such marked differences.
We have identified the immaturity of microvasculature and PB -associated capillaries with a pathological persistency of immature CD15+/CD31+/CD34+ endothelial cells and a reduction of terminally differentiated CD15-/CD31+/CD34+ endothelial cells in a structurally and clinically heterogeneous group of high weight-placentas. We assume that immaturity of placental vessels are part of prenatal adaptational processes that can be recruited in different emergency situations and may provide potential targets of therapeutic correction of placental growth and chronic insufficiency. We therefore recommend the use of CD15-based immunophenotyping as a method to identify latent unfavorable conditions of fetal development in the intrauterine life and individual risk of disease in the postnatal period.
孕龄期绒毛不成熟是一种多因素发育偏差，与意外的胎盘功能不全、胎儿缺氧和足月胎儿死亡相关。在我们之前的研究中，我们已经表明未成熟的CD15+/CD31+/CD34+内皮细胞是胎盘绒毛不成熟和慢性功能不全的重要指标。本研究的目的是对临床和结构上异质的正常、低体重和高体重足月胎盘的血管壁中CD15标记的不成熟情况进行比较分析。
对165例孕龄39 - 42周、体重正常（第25 - 75百分位数）、低体重（<第10百分位数）和高体重（>第90百分位数）的临床正常和病理胎盘进行结构和免疫组织化学分析。排除与宫内胎儿死亡、低阿氏评分、遗传和染色体疾病或胎盘炎症相关的严重胎盘功能不全形式的胎盘。分别在大血管、微血管和胎盘屏障（PB）相关毛细血管中评估CD15、CD31和CD34的分布模式。
所有体重正常、低体重和高体重的胎盘组均包括正常、加速的绒毛成熟或绒毛不成熟，与体重无关。然而，与正常体重（13.8%/8.2%）和低体重（16.1%/17.8%）的胎盘相比，高体重胎盘的微血管和PB相关毛细血管中未成熟的CD15+/CD31+/CD34+内皮细胞显著增加（63.5%/52.2%）。大血管未成熟的CD15+/CD31+/CD34+内皮细胞的分布没有显示出如此明显的差异。
我们在结构和临床异质的高体重胎盘组中，确定了微血管和PB相关毛细血管的不成熟，其特征为未成熟的CD15+/CD31+/CD34+内皮细胞的病理持续性以及终末分化的CD15-/CD31+/CD34+内皮细胞减少。我们假设胎盘血管的不成熟是产前适应过程的一部分，可在不同的紧急情况下被调用，并可能为胎盘生长和慢性功能不全提供治疗纠正的潜在靶点。因此，我们建议使用基于CD
