Down-regulated expressed protein HMGB3 inhibits proliferation and migration, promotes apoptosis in the placentas of fetal growth restriction

2019 ◽  
Vol 107 ◽  
pp. 69-76 ◽  
Author(s):  
Yan Lv ◽  
Mingming Lv ◽  
Xiaohong Ji ◽  
Lu Xue ◽  
Can Rui ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
And Migration ◽  
Proliferation And Migration

Decreased PGF may contribute to trophoblast dysfunction in fetal growth restriction

Reproduction ◽  
2017 ◽  
Vol 154 (3) ◽  
pp. 319-329 ◽  
Author(s):  
Wei-Bin Wu ◽  
Yue-Ying Xu ◽  
Wei-Wei Cheng ◽  
Bo Yuan ◽  
Jiu-Ru Zhao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Cpg Island ◽  
Growth Restriction ◽  
Trophoblastic Cell ◽  
Dna Methylation Profile ◽  
And Migration ◽  
Proliferation And Migration

Fetal growth restriction (FGR) threatens perinatal health and is correlated with increased incidence of fetal original adult diseases. Most cases of FGR were idiopathic, which were supposed to be associated with placental abnormality. Decreased circulating placental growth factor (PGF) was recognized as an indication of placental deficiency in FGR. In this study, the epigenetic regulation of PGF in FGR placentas and the involvement of PGF in modulation of trophoblast activity were investigated. The expression level of PGF in placental tissues was determined by RT-qPCR, immunohistochemistry and ELISA. DNA methylation profile ofPGFgene was analyzed by bisulfite sequencing. Trophoblastic cell lines were treated with ZM-306416, an inhibitor of PGF receptor FLT1, to observe the effect of PGF/FLT1 signaling on cell proliferation and migration. We demonstrated that PGF was downregulated in placentas from FGR pregnancies compared with normal controls. The villous expression of PGF was positively correlated with placental and fetal weight. The CpG island inside PGF promoter was hypomethylated without obvious difference in both normal and FGR placentas. However, the higher DNA methylation at another CpG island downstream exon 7 ofPGFwas demonstrated in FGR placentas. Additionally, we found FLT1 was expressed in trophoblast cells. Inhibition of PGF/FLT1 signaling by a selective inhibitor impaired trophoblast proliferation and migration. In conclusion, our data suggested that the PGF expression was dysregulated, and disrupted PGF/FLT1 signaling in trophoblast might contribute to placenta dysfunction in FGR. Thus, our results support the significant role of PGF in the pathogenesis of FGR.

scholarly journals Phosphorylation of Yes-associated protein impairs trophoblast invasion and migration: implications for the pathogenesis of fetal growth restriction†

2020 ◽  
Vol 103 (4) ◽  
pp. 866-879
Author(s):  
Hao Wang ◽  
Ping Xu ◽  
Xiaofang Luo ◽  
Mingyu Hu ◽  
Yamin Liu ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Cell Function ◽  
Hippo Pathway ◽  
Growth Restriction ◽  
Growth Potential ◽  
Biomechanical Analysis ◽  
Trophoblast Invasion ◽  
Invasion And Migration ◽  
And Migration

Abstract Fetal growth restriction (FGR) is a condition in which a newborn fails to achieve his or her prospective hereditary growth potential. This condition is associated with high newborn mortality, second only to that associated with premature birth. FGR is associated with maternal, fetal, and placental abnormalities. Although the placenta is considered to be an important organ for supplying nutrition for fetal growth, research on FGR is limited, and treatment through the placenta remains challenging, as neither proper uterine intervention nor its pathogenesis have been fully elucidated. Yes-associated protein (YAP), as the effector of the Hippo pathway, is widely known to regulate organ growth and cancer development. Therefore, the correlation of the placenta and YAP was investigated to elucidate the pathogenic mechanism of FGR. Placental samples from humans and mice were collected for histological and biomechanical analysis. After investigating the location and role of YAP in the placenta by immunohistochemistry, we observed that YAP and cytokeratin 7 have corresponding locations in human and mouse placentas. Moreover, phosphorylated YAP (p-YAP) was upregulated in FGR and gradually increased as gestational age increased during pregnancy. Cell function experiments and mRNA-Seq demonstrated impaired YAP activity mediated by extracellular signal-regulated kinase inhibition. Established FGR-like mice also recapitulated a number of the features of human FGR. The results of this study may help to elucidate the association of FGR development with YAP and provide an intrauterine target that may be helpful in alleviating placental dysfunction.

FETAL GROWTH RESTRICTION WITH EARLY AND LATE MANIFESTATION, PROGNOSTIC MARKERS

2020 ◽  
pp. 27-30
Author(s):  
Yakubova D.I.
Keyword(s):  
Risk Factors ◽  
Pregnant Women ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Prenatal Screening ◽  
Prognostic Markers ◽  
Growth Restriction ◽  
Late Manifestation ◽  
Late Form ◽  
Early Manifestation

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.

INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE

2018 ◽  
pp. 184-195
Author(s):  
Minh Son Pham ◽  
Vu Quoc Huy Nguyen ◽  
Dinh Vinh Tran
Keyword(s):  
Fetal Growth ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Growth Potential ◽  
National Guidelines ◽  
Intrauterine Growth ◽  
No Gold Standard

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)

The secrets of placental mosaicism: clinical observation of the full form of confined placental trisomy 22 and literature review

2020 ◽  
Author(s):  
I.V. Komarova, A.A. Nikiforenko, A.V. Fedunyak
Keyword(s):  
Prenatal Diagnosis ◽  
Literature Review ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Clinical Observation ◽  
Growth Restriction ◽  
Favorable Outcome ◽  
Full Form ◽  
Placental Mosaicism ◽  
In Pregnancy

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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