Angiotensin-1 and vimentin expression and ultrastructural examination in severe preeclampsia complicated by HELLP syndrome changes in the structure of the umbilical cord

• Published in: European review for medical and pharmacological sciences Vol. 27; no. 6; p. 2535
• Main Authors: Özgökçe, Ç, Öcal, A, Ermiş, I S, Deveci, E
• Format: Journal Article
• Language: English
• Published: Italy 01-03-2023
• Subjects: Endothelial Cells - metabolism; Female; HELLP Syndrome - metabolism; HELLP Syndrome - pathology; Humans; Pre-Eclampsia - pathology; Pregnancy; Umbilical Cord - metabolism; Vimentin
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_202303_31787

The purpose of this study was to examine the histopathologic, ultrastructural and immunohistochemical changes in the umbilical cord in women diagnosed with HELLP syndrome.
Postpartum umbilical cords of 40 patients at the 35-38th week of pregnancy were included. 20 severe preeclamptic (HELLP) and 20 normal umbilical cords were used. After the follow-up of tissue parts of 10% formaldehyde solution for histopathology and immunohistochemistry, histopathological and angiopoietin-1 and vimentin antibodies were examined as immunohistochemical after routine paraffin follow-up. For electron microscope analysis, umbilical cord samples were taken into 2.5% glutaral aldehyde solution.
In the statistical comparison, mean difference in increased diameter and additional anomaly on the ultrasound of preeclamptic patients was statistically different compared to control patients. In the HELLP group, hyperplasia and degenerative changes, pyknosis of the endothelial cell nuclei of the vessels and apoptotic changes in some regions were observed. Immunohistochemical analysis showed that endothelial cells, basal membrane and fibroblast cells in the HELLP group expressed high levels of vimentin. Angiotensin-1 expression was increased in amniotic epithelial cells, endothelial cells and some pericyte cells.
As a result, it was observed that the signaling that started with trophoblastic invasion with the effect of hypoxia in severe preeclampsia and continued with dysfunction in endothelial cells was parallel to the increase in angiotensin and vimentin receptors. It is thought that the ultrastructural change in endothelial cells may cause disruption of the collagenized structure in Wharton gel, which supports this, and may cause adverse effects in fetal development and nutrition.