scholarly journals Insight Into the Pathogenesis of Fetal Growth Restriction in Placental Malaria: Decreased Placental Glucose Transporter Isoform 1 Expression

2013 ◽  
Vol 209 (10) ◽  
pp. 1663-1667 ◽  
Author(s):  
Upeksha P. Chandrasiri ◽  
Caroline L. L. Chua ◽  
Alexandra J. Umbers ◽  
Ebbie Chaluluka ◽  
Jocelyn D. Glazier ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Glucose Transporter ◽  
Placental Malaria ◽  
Growth Restriction ◽  
Insight Into

scholarly journals Unique microRNA Signals in Plasma Exosomes from Pregnancies Complicated by Preeclampsia

Hypertension ◽  
2020 ◽  
Vol 75 (3) ◽  
pp. 762-771 ◽  
Author(s):  
Hui Li ◽  
Yingshi Ouyang ◽  
Elena Sadovsky ◽  
W. Tony Parks ◽  
Tianjiao Chu ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Quantitative Polymerase Chain Reaction ◽  
Growth Restriction ◽  
Differentially Expressed ◽  
Outcome Variable ◽  
Significant Difference ◽  
Exosomal Mirna ◽  
Plasma Mirna ◽  
Insight Into

Although preeclampsia is a common and serious complication of pregnancy, insight into its pathobiology and diagnosis is lacking. Circulating plasma exosomes, which contain RNA and other molecules and have recently become accessible for diagnostics, may be informative in this regard. We tested the hypothesis that preeclampsia may affect the miRNA cargo within circulating maternal blood exosomes. We collected plasma from 60 pregnant women at term, including 20 women with pregnancy complicated by preeclampsia, and 20 women with fetal growth restriction and 20 with healthy pregnancy, serving as controls. We isolated exosomes from the maternal plasma by continuous density gradient ultracentrifugation. Our main outcome variable was exosomal miRNA cargo, analyzed by quantitative polymerase chain reaction-based TaqMan advanced miRNA assay in a card format and the expression of differentially expressed exosomal miRNA in whole plasma from the same participants. We found that 7 miRNA species were differentially expressed in exosomes from women with preeclampsia and those from controls. In contrast, there was no significant difference in exosomal miRNA expression between women with fetal growth restriction and controls. The results were not affected by fetal sex. Only one of the preeclampsia-related, differentially expressed exosomal miRNAs was significantly different in whole plasma miRNA analysis. We concluded that unlike whole plasma miRNA, exosomes extracted from the plasma of women with preeclampsia exhibit a unique miRNA profile, suggesting that plasma exosomal miRNA could provide insight into the pathophysiology of preeclampsia, and may play a role in disease diagnostics.

Metallothionein-I- and -II-deficient mice display increased susceptibility to cadmium-induced fetal growth restriction

2013 ◽  
Vol 305 (6) ◽  
pp. E727-E735 ◽  
Author(s):  
Johanna Selvaratnam ◽  
Haiyan Guan ◽  
James Koropatnick ◽  
Kaiping Yang
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Structural Changes ◽  
Molecular Mechanisms ◽  
Glucose Transporter ◽  
Cadmium Exposure ◽  
Growth Restriction ◽  
Glut1 Expression ◽  
Pregnant Mice ◽  
Underlying Mechanisms

Maternal cadmium exposure induces fetal growth restriction (FGR), but the underlying mechanisms remain largely unknown. The placenta is the main organ known to protect the fetus from environmental toxins such as cadmium. In this study, we examine the role of the two key placental factors in cadmium-induced FGR. The first is placental enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which is known to protect the fetus from exposure to high cortisol levels and subsequently FGR, and the second the cadmium binding/sequestering proteins metallotheionein (MT)-I and -II. Using the MT-I/II −/− mouse model, pregnant mice were administered cadmium, following which pups and placentas were collected and examined. MT-I/II−/− pups exposed to cadmium were significantly growth restricted, but neither placental weight nor 11β-HSD2 was altered. Although cadmium administration did not result in any visible structural changes in the placenta, increased apoptosis was detected in MT-I/II−/− placentas following cadmium exposure, with a significant increase in levels of both p53 and caspase 3 proteins. Additionally, glucose transporter (GLUT1) was significantly reduced in MT-I/II−/− placentas of pups exposed to cadmium, whereas zinc transporter (ZnT-1) remained unaltered. Taken together, these results demonstrate that MT-I/II−/− mice are more vulnerable to cadmium-induced FGR. The present data also suggest that increased apoptosis and reduced GLUT1 expression in the placenta contribute to the molecular mechanisms underlying cadmium-induced FGR.

scholarly journals Circulating Soluble Endoglin Levels in Pregnant Women in Cameroon and Malawi—Associations with Placental Malaria and Fetal Growth Restriction

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24985 ◽  
Author(s):  
Karlee L. Silver ◽  
Andrea L. Conroy ◽  
Rose G. F. Leke ◽  
Robert J. I. Leke ◽  
Philomina Gwanmesia ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Placental Malaria ◽  
Growth Restriction ◽  
Soluble Endoglin

Effects of Antenatal Melatonin Treatment on the Cerebral Vasculature in an Ovine Model of Fetal Growth Restriction

2017 ◽  
Vol 39 (1-4) ◽  
pp. 323-337 ◽  
Author(s):  
Margie Castillo-Melendez ◽  
Tamara Yawno ◽  
Amy Sutherland ◽  
Graham Jenkin ◽  
Euan M. Wallace ◽  
...  
Keyword(s):  
White Matter ◽  
Blood Vessels ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Glucose Transporter ◽  
Growth Restriction ◽  
Periventricular White Matter ◽  
Cerebral Vasculature ◽  
Artery Ligation ◽  
Glucose Transporter 1

Chronic moderate hypoxia, such as occurs in fetal growth restriction (FGR) during gestation, compromises the blood-brain barrier (BBB) and results in structural abnormalities of the cerebral vasculature. We have previously determined the neuroprotective and antioxidant effects of maternal administration of melatonin (MLT) on growth-restricted newborn lambs. The potential of maternal MLT therapy for the treatment of cerebrovascular dysfunction-associated developmental hypoxia has also been demonstrated in newborn lambs. We assessed whether MLT had an effect on the previously reported structural and cerebral vascular abnormalities in chronically hypoxic FGR lambs. Single umbilical-artery ligation surgery was performed in fetuses at approximately 105 days of gestation (term: 147 days) to induce placental insufficiency and FGR, and treatment with either saline or an MLT infusion (0.1 mg/kg) was started 4 h after surgery. Ewes delivered naturally at term and lambs were euthanased 24 h later. We found a significant reduction in the number of laminin-positive blood vessels within the subcortical and periventricular white matter (SCWM and PVWM) and the subventricular zone (SVZ) in FGR (p < 0.0005) and FGR + MLT brains (p < 0.0005 vs. controls), with no difference found between FGR and FGR + MLT animals. This was associated with a significant decrease in VEGF immunoreactivity in FGR and FGR + MLT brains versus controls (p < 0.0005; SCWM and PVWM) and in the SVZ in FGR brains versus controls (p < 0.005) and also with significantly lower levels of proliferating blood vessels versus controls (p < 0.0005). Glucose transporter-1 immunoreactivity (vascular endothelium) was decreased in FGR versus control lambs (p < 0.0005) in SCWM, PVWM, and the SVZ; it was significantly increased in FGR + MLT lambs compared with FGR lambs in SCWM and PVWM (p < 0.005) and even more markedly in the SVZ (p < 0.0005). FGR brains showed a 72% reduction in pericyte coverage versus control lambs and 68% versus FGR + MLT in PVWM. In SCWM, we found a 77 and 73% reduction compared with control and FGR + MLT lambs, respectively, while in the SVZ, we observed a 68% reduction versus controls and a 70% reduction in FGR versus FGR + MLT lambs. Astrocyte end-feet coverage in the SCWM showed a significant 24% reduction in FGR versus control levels, a 42% decrease within the PVWM, and a 35% decrease within the SVZ versus controls. MLT normalized astrocyte attachment to blood vessels, with no difference seen between controls and FGR + MLT animals in any of the brain regions examined. We also observed a decrease in albumin extravasation and microhemorrhage in controls and FGR + MLT brains versus FGR lambs. Our results demonstrate that umbilicoplacental insufficiency is associated with FGR-produced vascular changes in the white matter and SVZ of FGR newborn brains and that maternal MLT prevented disruption of the BBB by protecting perivascular cells essential for the maintenance of vascular homeostasis and stability.

scholarly journals Complement Activation and the Resulting Placental Vascular Insufficiency Drives Fetal Growth Restriction Associated with Placental Malaria

2013 ◽  
Vol 13 (2) ◽  
pp. 215-226 ◽  
Author(s):  
Andrea L. Conroy ◽  
Karlee L. Silver ◽  
Kathleen Zhong ◽  
Monique Rennie ◽  
Peter Ward ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Complement Activation ◽  
Fetal Growth Restriction ◽  
Placental Malaria ◽  
Growth Restriction ◽  
Vascular Insufficiency

Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction

2007 ◽  
Vol 292 (5) ◽  
pp. E1241-E1255 ◽  
Author(s):  
Amit Ganguly ◽  
Robert A. McKnight ◽  
Santanu Raychaudhuri ◽  
Bo-Chul Shin ◽  
Zhigui Ma ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Fetal Growth ◽  
Early Pregnancy ◽  
Fetal Growth Restriction ◽  
Pregnancy Loss ◽  
Glucose Transporter ◽  
Growth Restriction ◽  
Late Gestation ◽  
Null Mouse ◽  
Early Pregnancy Loss

Glucose transporter isoform-3 (GLUT3) is the trophoblastic facilitative glucose transporter. To investigate the role of this isoform in embryonic development, we created a novel GLUT3-null mouse and observed arrested early embryonic development and loss at neurulation stage when both alleles were mutated. This loss occurred despite the presence of other related isoforms, particularly GLUT1. In contrast, when a single allele was mutated, despite increased embryonic cell apoptosis, adaptive changes in the subcellular localization of GLUT3 and GLUT1 in the preimplantation embryo led to postimplantation survival. This survival was compromised by decreased GLUT3-mediated transplacental glucose transport, causing late-gestation fetal growth restriction. This yielded young male and female adults demonstrating catch-up growth, with normal basal glucose, insulin, insulin-like growth factor-I and IGF-binding protein-3 concentrations, fat and lean mass, and glucose and insulin tolerance. We conclude that GLUT3 mutations cause a gene dose-dependent early pregnancy loss or late-gestation fetal growth restriction despite the presence of embryonic and placental GLUT1 and a compensatory increase in system A amino acid placental transport. This critical life-sustaining functional role for GLUT3 in embryonic development provides the basis for investigating the existence of human GLUT3 mutations with similar consequences during early pregnancy.

scholarly journals Syncytiotrophoblast Functions and Fetal Growth Restriction during Placental Malaria: Updates and Implication for Future Interventions

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Winifrida B. Kidima
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Placental Malaria ◽  
In Utero ◽  
Malaria Risk ◽  
Growth Restriction ◽  
Placental Pathology ◽  
Intervillous Space

Syncytiotrophoblast lines the intervillous space of the placenta and plays important roles in fetus growth throughout gestation. However, perturbations at the maternal-fetal interface during placental malaria may possibly alter the physiological functions of syncytiotrophoblast and therefore growth and development of the embryoin utero. An understanding of the influence of placental malaria on syncytiotrophoblast function is paramount in developing novel interventions for the control of placental pathology associated with placental malaria. In this review, we discuss how malaria changes syncytiotrophoblast function as evidenced from human, animal, andin vitrostudies and, further, how dysregulation of syncytiotrophoblast function may impact fetal growthin utero. We also formulate a hypothesis, stemming from epidemiological observations, that nutrition may override pathogenesis of placental malaria-associated-fetal growth restriction. We therefore recommend studies on nutrition-based-interventional approaches for high placental malaria-risk women in endemic areas. More investigations on the role of nutrition on placental malaria pathogenesis are needed.

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.

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