期刊
PLACENTA
卷 43, 期 -, 页码 69-76出版社
W B SAUNDERS CO LTD
DOI: 10.1016/j.placenta.2016.05.002
关键词
Glycocalyx; Glycocode; Lectin histochemistry; Placenta; Preeclampsia
资金
- grant Diagnostic and prognostic role of molecular, genetic, immunological, epigenetic factors of preeclampsia development (the Ministry of Education and Science of Russia)
Introduction: Glycans expressed in the fetal-maternal interface were shown to exert immunomodulating effects and to mediate interactions between the cells. The aim of this study was to investigate alterations in the structure of carbohydrate chains of glycocalyx in placental tissue in pregnancies complicated with preeclampsia (PE). Methods: A histochemical analysis of placental tissues was performed with a panel of biotinylated lectins. We analyzed placental tissues in women who had severe or moderate PE and compared them to placentas from women with normal pregnancies. Results: There was decreased content of terminal residues of alpha(2,6)-linked sialic acid (as stained by SNA lectin) in the carbohydrate chains of glycocalyx of the endothelium of placental terminal villi in patients with moderate preeclampsia. The composition of the glycocalyx of syncytiotrophoblast in patients of this group did not differ from the control group. Amount of the glycans with terminal beta-Gal-(ECL) and alpha-mannosyl residues (ConA) in the syncytiotrophoblast and capillary endothelium of the placenta was significantly higher in the group with severe PE compared to the control group. The increased content of sialoglycans with alpha(2,6)-linked sialic acids residues were discovered in the syncytium, and the decreased content of alpha(2,3)-linked sialic acids residues - in the endothelium of terminal villi in preeclampsia. Discussion: The most prominent alteration of the glycocalyx composition was found in the placentas of women with severe preeclampsia. It is likely that the modified glycome of syncytiotrophoblast and capillary endothelium may play an important role in pathogenesis of preeclampsia. (C) 2016 Elsevier Ltd. All rights reserved.
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