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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Comparative Characteristics of Sialoglycans Expression Disorders in the Placental Barrier Structures in Preeclampsia
M M Ziganshina1, G V Kulikova2, A I Shchegolev2
1V. I. Kulakov National Medical Research Center of Obstetrics, Gynecology, and Perinatology, Ministry of Health of the Russian Federation, Moscow, Russia. mmz@mail.ru.
We compared the expression profiles of α2,3- and α2,6-sialoglycans in the glycocalyx of the placental barrier structures in early and late forms of preeclampsia and fetal growth restriction using the method of lectin histochemistry. It was found that the expression of α2,3-sialoglycans in the syncytiotrophoblast and fetal endothelium of the terminal villi of the placenta was reduced in preeclampsia in comparison with normal placenta and, on the contrary, was increased in fetal growth restriction. Significant differences were found in both clinical phenotypes of preeclampsia and fetal growth restriction. Changes in the expression pattern of α2,6-sialoglycans in the endothelium of terminal villi were more pronounced than in syncytiotrophoblast. In early and late-onset preeclampsia, a significant increase in the expression of α2,6-sialoglycans was revealed only in the fetal endothelium; in early fetal growth restriction, the expression of α2,6-sialoglycans was reduced in the endothelium, but increased in syncytiotrophoblast in late fetal growth restriction. The features of the expression of sialoglycans in structures of the placental barrier in preeclampsia and fetal growth restriction were revealed, which may indicate the pathogenetic involvement of sialoglycans in the inflammatory activation cascade in fetal growth restriction, and in preeclampsia, apparently, they are associated with impaired fetal tolerance.
We compared the expression profiles of α2,3- and α2,6-sialoglycans in the glycocalyx of the placental barrier structures in early and late forms of preeclampsia and fetal growth restriction using the method of lectin histochemistry. It was found that the expression of α2,3-sialoglycans in the syncytiotrophoblast and fetal endothelium of the terminal villi of the placenta was reduced in preeclampsia in comparison with normal placenta and, on the contrary, was increased in fetal growth restriction. Significant differences were found in both clinical phenotypes of preeclampsia and fetal growth restriction. Changes in the expression pattern of α2,6-sialoglycans in the endothelium of terminal villi were more pronounced than in syncytiotrophoblast. In early and late-onset preeclampsia, a significant increase in the expression of α2,6-sialoglycans was revealed only in the fetal endothelium; in early fetal growth restriction, the expression of α2,6-sialoglycans was reduced in the endothelium, but increased in syncytiotrophoblast in late fetal growth restriction. The features of the expression of sialoglycans in structures of the placental barrier in preeclampsia and fetal growth restriction were revealed, which may indicate the pathogenetic involvement of sialoglycans in the inflammatory activation cascade in fetal growth restriction, and in preeclampsia, apparently, they are associated with impaired fetal tolerance.
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