Histopathological, ultrastructural, and immunohistochemical examination of changes in the placenta as a result of severe preeclampsia.

IF 1.1 4区 医学 Q3 SURGERY Acta cirurgica brasileira Pub Date : 2023-01-01 DOI:10.1590/acb382023
Çağdaş Özgökçe, Aydın Öcal, Işılay Seze Ermiş, Engin Deveci
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Abstract

Purpose: To investigate the role of hypoxia-inducible transcription factor-1 alpha (HIF-1α) and angiogenetic factor endothelin-1 (ET-1) expression in regulating hypoxia and placental development by routine histopathological methods.

Methods: Twenty preeclamptic and normal placentas were used. Placenta tissue pieces were examined histopathologically after routine paraffin follow-ups. HIF-1α and ET-1 proteins were examined immunohistochemically, and placental tissues were examined ultrastructurally.

Results: Increase in syncytial proliferation, endothelial damage in vessels, and increase in collagen were observed in preeclamptic placentas. As a result of preeclampsia, an increase was observed in HIF-1α and ET-1 protein levels in the placenta. Dilatation of endoplasmic reticulum and loss of cristae in mitochondria were observed in trophoblast cells in preeclamptic placental sections.

Conclusions: High regulation of oxygen resulting from preeclampsia has been shown to be a critical determinant of placentagenesis and plays an important role in placental differentiation, changes in maternal and fetal blood circulation, trophoblastic invasion, and syncytial node increase. It has been thought that preeclampsia affects secretion by disrupting the endoplasmic reticulum structure and induces mitochondrial damage, and that ET-1 may potentially help in the induction of stress pathways as a result of hypoxia in preeclampsia.

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重度子痫前期胎盘组织病理学、超微结构及免疫组化检查。
目的:通过常规组织病理学方法探讨缺氧诱导转录因子-1α (HIF-1α)和血管生成因子内皮素-1 (ET-1)表达在缺氧和胎盘发育中的作用。方法:选用子痫前期胎盘和正常胎盘各20例。常规石蜡随访后对胎盘组织切片进行组织病理学检查。免疫组化检测HIF-1α和ET-1蛋白,超微结构检测胎盘组织。结果:子痫前期胎盘合胞细胞增殖增加,血管内皮损伤,胶原蛋白增多。作为子痫前期的结果,胎盘中HIF-1α和ET-1蛋白水平升高。在子痫前期胎盘切片中观察到滋养细胞内质网扩张和线粒体嵴缺失。结论:先兆子痫导致的高氧调节已被证明是胎盘发生的关键决定因素,并在胎盘分化、母胎血液循环改变、滋养细胞侵袭和合胞结增加中起重要作用。人们一直认为,子痫前期通过破坏内质网结构和诱导线粒体损伤来影响分泌,ET-1可能潜在地帮助诱导子痫前期缺氧导致的应激途径。
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CiteScore
1.90
自引率
9.10%
发文量
60
审稿时长
3-8 weeks
期刊介绍: Information not localized
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