scholarly journals Placental Angiogenesis and Fetal Growth Restriction

Author(s):  
Victor Gourvas ◽  
Efterpi Dalpa ◽  
Nikos Vrachnis ◽  
Stavros Sifakis
2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Xueju Wang ◽  
Luyao Li ◽  
Pengbo Yuan ◽  
Yangyu Zhao ◽  
Yuan Wei

Abstract Background Unequal placental territory in monochorionic diamniotic twins is a primary cause of selective fetal growth restriction (sFGR), and vascular anastomoses play important role in determining sFGR prognosis. This study investigated differences in placental characteristics and pregnancy outcomes in cases of sFGR with and without thick arterio-arterial anastomosis (AAA). Methods A total of 253 patients diagnosed with sFGR between April 2013 and April 2020 were retrospectively analyzed. An AAA greater than 2 mm in diameter was defined as a thick AAA. We compared placental characteristics and pregnancy outcomes between cases of sFGR with and without thick AAA. Results Prevalence of AAA, thick arterio-venous anastomosis (AVA), veno-venous anastomosis (VVA), and thick VVA were significantly higher in the thick AAA group relative to the non-thick AAA group (100.0 vs. 78.5%, P < 0.001; 44.3 vs. 15.4%, P < 0.001; 27.1 vs. 10.8%, P = 0.017, and 24.3 vs. 6.2%, P = 0.004, respectively). The total numbers of AVA and total anastomoses were significantly higher in thick AAA group relative to the non-thick AAA group (5 [1, 14] vs. 3 [1, 15, P = 0.016; and 6 [1, 15] vs. 5 [1, 16], P = 0.022, respectively). The total diameter of AAA, AVA, VVA, and all anastomoses in the thick AAA group was larger than in the non-thick AAA group (3.4 [2.0,7.1] vs. 1.4 [0.0, 3.3], P < 0.001; 6.3 [0.3, 12.0] vs. 2.5 [0.3, 17.8], P < 0.001; 4.2±1.8 vs. 1.9±1.2, P =0.004; and 10.7 [3.2,22.4] vs. 4.4 [0.5, 19.3], P < 0.001, respectively). Growth-restricted fetuses in the thick AAA group exhibited significantly increased birthweight relative to those in thenon-thick AAA group (1570 (530, 2460)g vs. 1230 (610, 2480)g, p = 0.002). Conclusions In the placentas associated with sFGR, thick AAA can co-occur with thick AVA and VVA, and placental angiogenesis may differ significantly based upon whether or not thick AAA is present. The birth weights of growth-restricted fetuses in cases of sFGR with thick AAA are larger than in cases without thick AAA.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Jenny L Sones ◽  
Scott D Butler ◽  
Catherine E Isroff ◽  
Jeeyeon Cha ◽  
Sudhansu K Dey ◽  
...  

Preeclampsia (PE) presents as maternal hypertension and proteinuria during the second half of pregnancy and often results in preterm delivery of a growth restricted baby. Despite being a leading cause of perinatal and maternal morbidity/mortality, the underlying mechanism(s) is unknown. Because signs resolve upon delivery of the placenta, abnormal placentation is widely accepted as the cause of PE. BPH/5 mice spontaneously develop the cardinal features of PE along with poor fetoplacental outcomes, such as fetal growth restriction. We have shown that BPH/5 implantation sites exhibit significant up-regulation of Ptgs2 (the gene encoding Cox2) at e7.5 as compared to C57. Since Cox2 and Cox2-derived prostaglandins (PGs) are crucial for uterine decidualization and placental angiogenesis, we tested the hypothesis that BPH/5 mice have dysregulated PG synthesis during decidualization and that this contributes to poor fetoplacental outcomes. Because e7.5 is considered the peak of decidualization, we designed experiments to selectively target Cox2 at this time in BPH/5 implantation sites. Administration of celecoxib by oral gavage at e6.5 (10mg/kg BW) caused a 2-fold reduction in Cox2 protein expression in BPH/5 implantation sites at e7.5 (n=3-4; p<0.05 vs BPH/5 veh). This had no effect on Cox2 levels in C57. This was associated with a significant reduction in PGE 2 synthesis (51.6±17.3 vs veh: 135.6±49.7 pg/mg), but not PGI 2 in e7.5 BPH/5 implantation sites (n=4-5; p<0.05). Neither PGE 2 nor PGI 2 synthesis was altered in C57 implantation sites. Furthermore, celecoxib improved fetal growth restriction in BPH/5 pups at e18.5 (1.108±0.091 vs veh: 1.036±0.021g), which was associated with an increase in placental weight (99.7±1.6 vs veh: 91.32±2.2mg) in BPH/5 females (n=20-38; p<0.05). These results provide evidence that Cox2 and PGE 2 play a key role in fetoplacental development in a mouse model of PE, and that celecoxib improves fetal outcomes in BPH/5 females. This highlights the significance of proper decidual angiogenesis and suggests that aberrations in these processes in early pregnancy may contribute to fetal growth restriction seen in PE pregnancies.


2019 ◽  
Vol 133 (12) ◽  
pp. 1353-1365
Author(s):  
Shuhan Ji ◽  
Hong Xin ◽  
Emily J. Su

Abstract Pregnancies complicated by severe fetal growth restriction with abnormal umbilical artery Doppler velocimetry (FGRadv) are at substantial risk for adverse perinatal and long-term outcomes. Impaired angiogenesis of the placental vasculature in these pregnancies results in a sparse, poorly branched vascular tree, which structurally contributes to the abnormally elevated fetoplacental vascular resistance that is clinically manifested by absent or reversed umbilical artery Doppler indices. Previous studies have shown that aryl hydrocarbon receptor nuclear translocator (ARNT) is a key mediator of proper placental angiogenesis, and within placental endothelial cells (ECs) from human FGRadv pregnancies, low expression of ARNT leads to decreased vascular endothelial growth factor A (VEGFA) expression and deficient tube formation. Thus, the aim of the present study was to determine the effect of VEGFA administration or ARNT overexpression on angiogenic potential of FGRadv ECs. ECs were isolated and cultured from FGRadv or gestational age-matched control placentas and subjected to either vehicle vs VEGFA treatment or transduction with adenoviral-CMV (ad-CMV) vs adenoviral-ARNT (ad-ARNT) constructs. They were then assessed via wound scratch and tube formation assays. We found that VEGFA administration nominally improved FGRadv EC migration (P<0.01) and tube formation (P<0.05). ARNT overexpression led to significantly enhanced ARNT expression in FGRadv ECs (P<0.01), to a level similar to control ECs. Despite this, FGRadv EC migration (P<0.05) and tube formation (P<0.05) were still only partially rescued. This suggests that although ARNT does play a role in fetoplacental EC migration, other factors in addition to ARNT are likely also important in placental angiogenesis.


Author(s):  
Yakubova D.I.

Objective of the study: Comprehensive assessment of risk factors, the implementation of which leads to FGR with early and late manifestation. To evaluate the results of the first prenatal screening: PAPP-A, B-hCG, made at 11-13 weeks. Materials and Methods: A retrospective study included 110 pregnant women. There were 48 pregnant women with early manifestation of fetal growth restriction, 62 pregnant women with late manifestation among them. Results of the study: The risk factors for the formation of the FGR are established. Statistically significant differences in the indicators between groups were not established in the analyses of structures of extragenital pathology. According to I prenatal screening, there were no statistical differences in levels (PAPP-A, b-hCG) in the early and late form of FGR.


2018 ◽  
pp. 184-195
Author(s):  
Minh Son Pham ◽  
Vu Quoc Huy Nguyen ◽  
Dinh Vinh Tran

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)


Author(s):  
I.V. Komarova, A.A. Nikiforenko, A.V. Fedunyak

Literature reports of placental mosaicism, including trisomy 22, were analyzed. The chance of correlation of placental aneuploidy with fetus aneuploidy, also the probability of complications in pregnancy and fetal growth restriction and postnatal patients growth in the cases of confined placental mosaicism, were demonstrated. The case of prenatal diagnosis of confined placental mosaicism of trisomy 22 with favorable outcome is presented. The necessity of cytogenic assay of amniocytes and fetal lymphocytes in the case of placental heteroploidy diagnosis was emphasized.


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