Regulation of Uterine Spiral Artery Remodeling: a Review

Albrecht, Eugene D.; Pepe, Gerald J.

doi:10.1007/s43032-020-00212-8

Cited by 58 publications

(41 citation statements)

References 181 publications

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“…Although anti-miR-210-3p was able to increase cell migration, invasion and EVT outgrowth, it only significantly increased the branching points at 48 h and did not significantly increase enEVT marker mRNA levels. Since many factors are involved in promoting spiral artery remodeling [44,45], it is likely that partial inhibition of endogenous miR-210-3p alone is insufficient to increase angiogenic potential and enEVT marker expression.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-210-3p Impairs Extravillous Trophoblast Functions Associated with Uterine Spiral Artery Remodeling

Hayder

Nadeem

et al. 2021

IJMS

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Hsa-miR-210-3p has been reported to be upregulated in preeclampsia (PE); however, the functions of miR-210-3p in placental development are not fully understood, and, consequently, miR-210-3p’s role in the pathogenesis of PE is still under investigation. In this study, we found that overexpression of miR-210-3p reduced trophoblast migration and invasion, extravillous trophoblast (EVT) outgrowth in first trimester explants, expression of endovascular trophoblast (enEVT) markers and the ability of trophoblast to form endothelial-like networks. In addition, miR-210-3p overexpression significantly downregulated the mRNA levels of interleukin-1B and -8, as well as CXC motif ligand 1. These cytokines have been suggested to play a role in EVT invasion and the recruitment of immune cells to the spiral artery remodeling sites. We also showed that caudal-related homeobox transcription factor 2 (CDX2) is targeted by miR-210-3p and that CDX2 downregulation mimicked the observed effects of miR-210-3p upregulation in trophoblasts. These findings suggest that miR-210-3p may play a role in regulating events associated with enEVT functions and its overexpression could impair spiral artery remodeling, thereby contributing to PE.

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Section: Discussionmentioning

confidence: 99%

Overexpression of miR-210-3p Impairs Extravillous Trophoblast Functions Associated with Uterine Spiral Artery Remodeling

Hayder

Nadeem

et al. 2021

IJMS

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“…The diagnostic criteria for PE is systolic blood pressure (SBP) ≥ 140 mm Hg and/or diastolic blood pressure (DBP) ≥ 90 mm Hg, accompanied by proteinuria and/or impairment of maternal vital organ function, or fetal growth restriction 2 . During the early stages of normal pregnancy, the extravillous trophoblasts gradually invade and replace the vascular smooth muscle cells and endothelial cells in the uterine spiral arteries, a process known as spiral artery remodelling 3 . The pathogenesis of PE is characterized by the reduction of placental perfusion caused by shallow placental implantation, which is a consequence of disorders in spiral artery remodelling.…”

Section: Introductionmentioning

confidence: 99%

Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks

Yin

Zhang

et al. 2021

J Cellular Molecular Medi

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Our previous studies have confirmed that lncRNA‐ATB may be involved in the pathogenesis of preeclampsia, however, it is uncertain whether lncRNA‐ATB influence the interaction between trophoblast and endothelial cells, which is crucial to the uterine spiral artery remodelling. Scratch wound healing and transwell invasion assay were conducted to test the migration and invasion of trophoblast cells. Co‐culture model was used to simulate the physiological environment in vivo. The expression levels of lncRNA‐ATB were analyzed in placenta tissues from healthy pregnant women and preeclampsia patients. Subsequently, the binding site of lncRNA‐ATB and miR‐651‐3p was verified using dual‐luciferase reporter assay, and the rescue experiment was used to study the effects of these two on the biological function. The direct effects of miR‐651‐3p and Yin Yang 1 (YY1) were verified using similar methods. LncRNA‐ATB was found to be down‐regulated in the placenta of preeclampsia patients. LncRNA‐ATB knockdown decreased trophoblast migration, invasion and colocalisation with human umbilical vein endothelial cells. MiR‐651‐3p was a direct target of lncRNA‐ATB and they had opposite effects. Moreover, the expression of lncRNA‐ATB and miR‐651‐3p in placental tissues was negatively correlated. MiR‐651‐3p has been confirmed to directly target the 3′ untranslated region of YY1. The inhibitory effects of YY1 low expression on biological function was rescued by miR‐651‐3p depletion. Western blot analysis showed that lncRNA‐ATB could regulate YY1 expression by sponging miR‐651‐3p. LncRNA‐ATB functioned as a competitive endogenous RNA of miR‐651‐3p to regulate YY1 on progress of spiral artery remodelling.

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“…Complications of anticoagulant therapy in pregnancy include embryopathy (nasal hypoplasia, spotted epiphyses), CNS abnormalities (Dandy-Walker syndrome, visual atrophy), fetal bleeding, hemorrhagic manifestations, skin allergies, thrombocytopenia and osteoporosis [60][61][62][63][64][65][66][67][68][69][70][71][72].…”

Section: When Will We Check a Patient For Aplsmentioning

confidence: 99%

Antiphospholipid Syndrome and Pregnancy-Diagnosis, Complications and Management: An Overview

Tsikouras¹,

Tsiggalou²,

Bothou³

et al. 2022

Inflammation in the 21st Century

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Antiphospholipid syndrome which is also known as APS is an autoimmune disease which represents an acquired form of thrombophilia. The etiology of APS remains unknown. This disorder occurs when the immune system mistakenly attacks some of the normal human proteins and manifests itself as recurrent arterial or venous thrombosis and it could emerge after abortions or in recurrent pregnancy loss. In APS, the body produces the wrong antibodies against phospholipid-binding proteins, that is present in the blood and plays an important role in coagulation. Antibodies are specific proteins that usually target and neutralize the body’s invaders, such as viruses and bacteria. When antibodies attack phospholipid-binding proteins, blood clots abnormally. Specifically, it could cause blood clots in veins or arteries leading to stroke and various pregnancy complications such as: endometrial death, miscarriage, preeclampsia, intrauterine growth restriction and prematurity. APS is divided into primary and secondary, which is associated with autoimmune diseases and more often with systemic lupus erythematosus (SLE), while antibodies against cardiolipin are detected in many other conditions (infections, malignancies, drugs, etc.). The symptoms of APS, in addition to arterial and/or venous thrombosis and pregnancy complications, are multisystemic and the differential diagnosis of the primary APS from the secondary, in the context of SLE, is of particular clinical interest and is subject of this literature review.

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Regulation of Uterine Spiral Artery Remodeling: a Review

Cited by 58 publications

References 181 publications

Overexpression of miR-210-3p Impairs Extravillous Trophoblast Functions Associated with Uterine Spiral Artery Remodeling

Overexpression of miR-210-3p Impairs Extravillous Trophoblast Functions Associated with Uterine Spiral Artery Remodeling

Effect of lncRNA‐ATB/miR‐651‐3p/Yin Yang 1 pathway on trophoblast‐endothelial cell interaction networks

Antiphospholipid Syndrome and Pregnancy-Diagnosis, Complications and Management: An Overview

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