Endovascular trophoblast and spiral artery remodeling. (1st March 2020)

• Record Type: Journal Article
• Authors: Sato, Yukiyasu
• Is Part Of: Molecular and cellular endocrinology. Volume 503(2020)
• Publication Date: 2020-03-01
• Subjects: Decidual natural killer cell -- Extravillous trophoblast -- Fetal growth restriction -- Interstitial trophoblast -- Oxygen -- Platelet -- Preeclampsia; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2019.110699
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Spiral artery remodeling, which is indispensable for successful pregnancy, is accomplished by endovascular trophoblasts that move upstream along the arterial wall, replace the endothelium, and disrupt the muscular lining. This review outlines the possible factors that could regulate endovascular trophoblast differentiation and invasion. First, high oxygen tension in the spiral artery could initiate endovascular trophoblast invasion. Second, activation of maternal decidual natural killer (dNK) cells could support perivascular invasion of interstitial trophoblasts and consequently could facilitate the endovascular trophoblast invasion. Third, maternal platelets trapped by the endovascular trophoblasts could enhance endovascular trophoblast invasion, which is in part mediated by chemokine CCL5 (C–C motif ligand 5) released from the activated platelets and chemokine receptor CCR1 (C–C chemokine receptor type 1) expressed specifically on the endovascular trophoblasts. The rat, in which trophoblast cells exhibit extensive interstitial and endovascular invasion, could be a suitable model animal for the study of human spiral artery remodeling. Apparently paradoxical results came from the rat study, i.e., exposure to hypoxia or depletion of dNK cells resulted in acceleration of the endovascular trophoblast invasion. This implies the presence of as-yet-undetermined regulator(s) whose effects on endovascular trophoblast invasion surpass the effects of surrounding oxygen tension or maternal dNK cells. In the future, clarification of the molecular differences between human interstitial and endovascular trophoblasts as well as establishment of the pregnant rat model exhibiting shallow endovascular trophoblast invasion and preeclamptic symptoms will contribute to elucidating the mechanism of spiral artery remodeling. Highlights: Spiral artery remodeling is accomplished by endovascular trophoblast invasion. High oxygen tension in spiral artery initiates endovascular trophoblast invasion. Activation of maternal dNK cells facilitates endovascular trophoblast invasion. Maternal platelets trapped by the endovascular trophoblasts enhance their invasion.