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. 2022 Dec;507(1):256-263.
doi: 10.1134/S1607672922060011. Epub 2022 Dec 29.

Regulation of the Placental Renin-Angiotensin-Aldosterone System in Early- and Late-Onset Preeclampsia

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Regulation of the Placental Renin-Angiotensin-Aldosterone System in Early- and Late-Onset Preeclampsia

K A Artemieva et al. Dokl Biochem Biophys. 2022 Dec.

Abstract

Preeclampsia (PE) is one of the most dangerous complications of pregnancy, characterized by hypertension, proteinuria, and symptoms of multiple organ failure, which are detected de novo after 20 weeks of pregnancy. The renin-angiotensin-aldosterone system (RAAS) is one of the first to recognize pregnancy and is an important regulator of blood pressure. The placenta has its own RAAS, the role of which in the development of PE is not fully understood. In this work, for the first time, we characterized the expression of RAAS components and miRNAs controlling it in the placenta at various times of PE manifestation. The data obtained will allow the development of a new strategy in the future for the search for therapeutic agents for patients suffering from PE and cardiovascular diseases.

Keywords: miRNA; placenta; preeclampsia; renin–angiotensin–aldosterone system.

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Conflict of interest statement

Conflict of interest. The authors declare that they have no conflicts of interest.

Figures

Fig. 1.
Fig. 1.
Expression of angiotensins in the placental villous tree in early- and late-onset preeclampsia (PE), ×400. (a) Early-onset PE (31–32 weeks), expression is noted in the syncytiotrophoblast (marked with a yellow arrow) and syncytial nodules (marked with a black arrow); (b) early comparison group (31 weeks); (c) late-onset PE (38 weeks); (d) late comparison group (38 weeks).
Fig. 2.
Fig. 2.
Expression of angiotensins in the decidua in early- and late-onset preeclampsia (PE), ×400. (a) Early-onset PE (32 weeks); (b) early comparison group (31 weeks); (c) late-onset PE (38 weeks); (d) late comparison group (38 weeks) (decidual cells are marked with arrows).
Fig. 3.
Fig. 3.
Expression of angiotensins in the structures of the placenta in early and late preeclampsia (PE): (a, b) in syncytiotrophoblast (a—membrane staining, b—cytoplasmic staining); (c, d) in the extravillous trophoblast (c—membrane staining, d—cytoplasmic staining); (e, f) in syncytial nodules (e—membrane staining, f—cytoplasmic staining); (g, h) in decidual cells (g—membrane staining, h—cytoplasmic staining); (i) cytoplasmic staining in the endothelium; (j) in fibroblast-like cells, cytoplasmic staining; (k, l) in macrophages (k—membrane staining, l—cytoplasmic staining). * Differences are significant in comparison with the control group; # differences are significant between the groups of early- and late-onset preeclampsia; ^ differences are significant between the groups of early and late norm.
Fig. 3.
Fig. 3.
(Contd.)

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