scholarly journals Maternal Choline Supplementation Alters Fetal Growth Patterns in a Mouse Model of Placental Insufficiency

Nutrients ◽  
2017 ◽  
Vol 9 (7) ◽  
pp. 765 ◽  
Author(s):  
Julia King ◽  
Sze Kwan ◽  
Jian Yan ◽  
Kevin Klatt ◽  
Xinyin Jiang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Fetal Growth ◽  
Growth Patterns ◽  
Placental Insufficiency

scholarly journals Maternal Choline Supplementation Modulates Placental Markers of Inflammation, Angiogenesis, and Apoptosis in a Mouse Model of Placental Insufficiency

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 374 ◽  
Author(s):  
Julia King ◽  
Sze Kwan ◽  
Jian Yan ◽  
Xinyin Jiang ◽  
Vladislav Fomin ◽  
...  
Keyword(s):  
Mouse Model ◽  
Litter Size ◽  
Fetal Growth ◽  
Placental Insufficiency ◽  
Dependent Manner ◽  
Fetal Sex ◽  
Placental Function ◽  
Markers Of Inflammation ◽  
Angiogenic Genes ◽  
Fetal Genotype

Dlx3 (distal-less homeobox 3) haploinsufficiency in mice has been shown to result in restricted fetal growth and placental defects. We previously showed that maternal choline supplementation (4X versus 1X choline) in the Dlx3+/− mouse increased fetal and placental growth in mid-gestation. The current study sought to test the hypothesis that prenatal choline would modulate indicators of placenta function and development. Pregnant Dlx3+/− mice consuming 1X (control), 2X, or 4X choline from conception were sacrificed at embryonic (E) days E10.5, E12.5, E15.5, and E18.5, and placentas and embryos were harvested. Data were analyzed separately for each gestational day controlling for litter size, fetal genotype (except for models including only +/− pups), and fetal sex (except when data were stratified by this variable). 4X choline tended to increase (p < 0.1) placental labyrinth size at E10.5 and decrease (p < 0.05) placental apoptosis at E12.5. Choline supplementation decreased (p < 0.05) expression of pro-angiogenic genes Eng (E10.5, E12.5, and E15.5), and Vegf (E12.5, E15.5); and pro-inflammatory genes Il1b (at E15.5 and 18.5), Tnfα (at E12.5) and Nfκb (at E15.5) in a fetal sex-dependent manner. These findings provide support for a modulatory effect of maternal choline supplementation on biomarkers of placental function and development in a mouse model of placental insufficiency.

scholarly journals Genomic imbalances in the placenta are associated with poor fetal growth

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Giulia F. Del Gobbo ◽  
Yue Yin ◽  
Sanaa Choufani ◽  
Emma A. Butcher ◽  
John Wei ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Sex Chromosome ◽  
Copy Number Variants ◽  
Placental Insufficiency ◽  
Potential Contribution ◽  
Genomic Imbalances ◽  
Significant Difference ◽  
Underlying Causes ◽  
Risk Of Disease ◽  
The Impact

Abstract Background Fetal growth restriction (FGR) is associated with increased risks for complications before, during, and after birth, in addition to risk of disease through to adulthood. Although placental insufficiency, failure to supply the fetus with adequate nutrients, underlies most cases of FGR, its causes are diverse and not fully understood. One of the few diagnosable causes of placental insufficiency in ongoing pregnancies is the presence of large chromosomal imbalances such as trisomy confined to the placenta; however, the impact of smaller copy number variants (CNVs) has not yet been adequately addressed. In this study, we confirm the importance of placental aneuploidy, and assess the potential contribution of CNVs to fetal growth. Methods We used molecular-cytogenetic approaches to identify aneuploidy in placentas from 101 infants born small-for-gestational age (SGA), typically used as a surrogate for FGR, and from 173 non-SGA controls from uncomplicated pregnancies. We confirmed aneuploidies and assessed mosaicism by microsatellite genotyping. We then profiled CNVs using high-resolution microarrays in a subset of 53 SGA and 61 control euploid placentas, and compared the load, impact, gene enrichment and clinical relevance of CNVs between groups. Candidate CNVs were confirmed using quantitative PCR. Results Aneuploidy was over tenfold more frequent in SGA-associated placentas compared to controls (11.9% vs. 1.1%; p = 0.0002, OR = 11.4, 95% CI 2.5–107.4), was confined to the placenta, and typically involved autosomes, whereas only sex chromosome abnormalities were observed in controls. We found no significant difference in CNV load or number of placental-expressed or imprinted genes in CNVs between SGA and controls, however, a rare and likely clinically-relevant germline CNV was identified in 5.7% of SGA cases. These CNVs involved candidate genes INHBB, HSD11B2, CTCF, and CSMD3. Conclusions We conclude that placental genomic imbalances at the cytogenetic and submicroscopic level may underlie up to ~ 18% of SGA cases in our population. This work contributes to the understanding of the underlying causes of placental insufficiency and FGR, which is important for counselling and prediction of long term outcomes for affected cases.

scholarly journals C-reactive protein levels in early pregnancy, fetal growth patterns, and the risk for neonatal complications: the Generation R Study

2011 ◽  
Vol 205 (2) ◽  
pp. 132.e1-132.e12 ◽  
Author(s):  
Gesina D.S. Ernst ◽  
Layla L. de Jonge ◽  
Albert Hofman ◽  
Jan Lindemans ◽  
Henk Russcher ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Early Pregnancy ◽  
Growth Patterns ◽  
C Reactive Protein ◽  
Neonatal Complications ◽  
Protein Levels ◽  
Reactive Protein

scholarly journals CD68+ M1 MACROPHAGES IS ASSOCIATED WITH PLACENTAL INSUFFICIENCY UNDER FETAL GROWTH RESTRICTION

2021 ◽  
Vol 74 (2) ◽  
pp. 213-219
Author(s):  
Varvara A. Berezhna ◽  
Tetiana V. Mamontova ◽  
Antonina M. Gromova
Keyword(s):  
Fetal Growth ◽  
Gestational Age ◽  
Fetal Growth Restriction ◽  
Preterm Births ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Immunohistochemical Method ◽  
Control Group ◽  
Stromal Component ◽  
Term Births

The aim: To elucidate the possible involvement of M1 and M2 macrophages in the placentas of women, whose pregnancies were complicated by fetal growth restriction (FGR) and resulted in term births after 37 weeks of gestation and preterm births up to 37 weeks of gestation. Materials and methods: CD68+ and CD163+ macrophages were studied by immunohistochemical method, placental morphology in the placentas of 16 women whose pregnancies were complicated by FGR and resulted in term births at a gestational age after 37 weeks (1-st group, n = 7) or resulted in preterm births at a gestational age up to 37 weeks (2-nd group, n = 9). The control group consisted of 10 placentas of women with physiological pregnancies and births. Results: Women 2-nd group showed significantly low weight of the placenta, a short gestation period at the time of delivery, and a prolonged labor period than women of the control group (p <0.001; p <0.001; p <0.05, respectively). The level of CD68+ and CD163+ macrophages in the placentas of women 2-nd group was significantly higher than in woman 1-st group (p <0.001, p <0.001, respectively). A significant correlation was found between the expression level of CD68+ monocytes in the intervillous space and the weight of a newborn (r = – 0.765; p = 0.016) in women 2-nd group. Conclusions: These studies suggest that in the placentas of women whose pregnancies were complicated by FGR and resulted in preterm births, the increased activation of CD68+ macrophages of the pro-inflammatory pool may be associated with disorders of the vascular and stromal component of the villous chorion with the development of involutive and dystrophic changes. In general, this fact probably determines the progress of chronic placental insufficiency and aggravates the development of fetal growth restriction.

scholarly journals Fetal Growth Patterns in Pregnancies With First-Trimester Bleeding

2018 ◽  
Vol 131 (6) ◽  
pp. 1021-1030 ◽  
Author(s):  
Alaina M. Bever ◽  
Sarah J. Pugh ◽  
Sungduk Kim ◽  
Roger B. Newman ◽  
William A. Grobman ◽  
...  
Keyword(s):  
Fetal Growth ◽  
First Trimester ◽  
Growth Patterns
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