Department of Obstetrics, Gynecology and Reproductive Sciences, Rutgers University Robert Wood Johnson School of Medicine, New Brunswick, NJ, USA.
Center for Perinatal Research, Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, OH, USA.
BJOG. 2018 Oct;125(11):1441-1448. doi: 10.1111/1471-0528.15176. Epub 2018 Apr 15.
Placenta accreta is clinically associated with maternal uterine scar. Our objective was to investigate the biochemical contribution of maternal scarring to hyperinvasive trophoblast. We hypothesised that trophoblast over-invasion in placenta accreta is associated with aberrant invasion-site signalling of growth and angiogenic factors known to be involved in wound healing and promotion of cell invasion through the epithelial to mesenchymal cellular programme.
Cross-sectional series.
Yale-New Haven Hospital.
Women with histologically confirmed normal and abnormal placentation.
Placental invasion site tissue sections were immunostained for endoglin and other angiogenic regulators, and transforming growth factor β (TGFβ) proteins. Maternal serum endoglin, and the vascular endothelial growth factor (VEGF) mediators hypoxia-inducible factor-1α (HIF1α) and endostatin, were assessed using immunoassay.
Differences in median H-score by immunostaining and in mean serum level by immunoassay.
By immunostaining, placenta accreta samples demonstrated intervillous endoglin shedding and increased trophoblast expression of its cleavage protein matrix metalloproteinase-14. Absent decidual HIF1α and endostatin were observed in areas of VEGF upregulation. TGFβ1 was present in myocytes but not in collagen bundles into which accreta trophoblast invaded. Maternal serum endoglin decreased in praevia and accreta when corrected for gestational age.
Angiogenic and growth factors at the placental invasion site are altered in accreta, both by decidual absence and within myometrial scar. We postulate this promotes the invasive phenotype of placenta accreta by activating hyperinvasive trophoblast and by dysregulating placental vascular remodelling.
Yale Department of Obstetrics, Gynecology and Reproductive Sciences funds.
Placenta accreta histology shows dysregulation of angiogenic and growth factors.
胎盘植入与产妇子宫瘢痕密切相关。我们的目的是研究产妇瘢痕对过度侵袭性滋养细胞的生化贡献。我们假设胎盘植入中滋养细胞的过度侵袭与已知参与伤口愈合和通过上皮到间充质细胞程序促进细胞侵袭的生长和血管生成因子的异常侵袭部位信号有关。
横截面系列。
耶鲁-纽黑文医院。
组织学证实正常和异常胎盘的女性。
胎盘侵袭部位组织切片免疫染色内皮糖蛋白和其他血管生成调节剂，以及转化生长因子β（TGFβ）蛋白。使用免疫测定法评估产妇血清内皮糖蛋白以及血管内皮生长因子（VEGF）介质缺氧诱导因子-1α（HIF1α）和内皮抑素。
免疫染色的中位数 H 评分差异和免疫测定的平均血清水平差异。
通过免疫染色，胎盘植入样本显示绒毛间内皮糖蛋白脱落和滋养细胞表达其裂解蛋白基质金属蛋白酶-14 增加。在 VEGF 上调区域观察到无蜕膜 HIF1α 和内皮抑素。TGFβ1 存在于肌细胞中，但不存在于植入滋养细胞侵入的胶原束中。校正妊娠年龄后，前置胎盘和植入胎盘产妇血清内皮糖蛋白减少。
植入部位的血管生成和生长因子既存在于蜕膜缺失中，也存在于子宫瘢痕中，都发生了改变。我们推测这通过激活过度侵袭性滋养细胞和调节胎盘血管重塑来促进胎盘植入的侵袭表型。
耶鲁大学妇产科和生殖科学系资助。
胎盘植入组织学显示血管生成和生长因子失调。
