scholarly journals Intrauterine growth restriction, human placental development and trophoblast cell death

2009 ◽  
Vol 587 (14) ◽  
pp. 3453-3458 ◽  
Author(s):  
Christina M. Scifres ◽  
D. Michael Nelson
Keyword(s):  
Cell Death ◽  
Intrauterine Growth Restriction ◽  
Trophoblast Cell ◽  
Growth Restriction ◽  
Placental Development ◽  
Intrauterine Growth

Influence of Maternal Dietary Intake, Intrauterine Growth Restriction (IUGR), and Estrogen Replacement on Placental Development and Vascularity.

2011 ◽  
Vol 85 (Suppl_1) ◽  
pp. 801-801 ◽  
Author(s):  
Roza D. Yunusova ◽  
Raymond P. Aitken ◽  
John S. Milne ◽  
Pawel Piotr Borowicz ◽  
Lawrence P. Reynolds ◽  
...  
Keyword(s):  
Dietary Intake ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Estrogen Replacement ◽  
Placental Development ◽  
Intrauterine Growth ◽  
Maternal Dietary Intake

scholarly journals Placental Expressions of CDKN1C and KCNQ1OT1 in Monozygotic Twins with Selective Intrauterine Growth Restriction

2017 ◽  
Vol 20 (5) ◽  
pp. 389-394 ◽  
Author(s):  
Chenyu Gou ◽  
Xiangzhen Liu ◽  
Xiaomei Shi ◽  
Hanjing Chai ◽  
Zhi-ming He ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mrna Expression ◽  
Intrauterine Growth Restriction ◽  
Monozygotic Twins ◽  
Growth Restriction ◽  
Control Group ◽  
Placental Development ◽  
Intrauterine Growth ◽  
Immunohistochemical Assay ◽  
Mrna Ratio

CDKN1C and KCNQ1OT1 are imprinted genes that might be potential regulators of placental development. This study investigated placental expressions of CDKN1C and KCNQ1OT1 in monozygotic twins with and without selective intrauterine growth restriction (sIUGR). Seventeen sIUGR and fifteen normal monozygotic(MZ) twin pairs were examined. Placental mRNA expressions of CDKN1C and KCNQ1OT1 were detected by real-time fluorescent quantitative PCR. CDKN1C protein expression was detected by immunohistochemical assay and Western-blotting. In the sIUGR group, smaller fetuses had a smaller share of the placenta, and CDKN1C protein expression was significantly increased while KCNQ1OT1 mRNA expression was significantly decreased. The CDKN1C/KCNQ1OT1 mRNA ratio was lower in the larger fetus than in the smaller fetus (p < .05). In the control group, CDKN1C protein expression showed no difference between larger and smaller fetuses, while KCNQ1OT1 mRNA expression was significantly lower in the larger fetus, and the CDKN1C/KCNQ1OT1 mRNA ratio was higher in the larger fetus than in the smaller fetus (p < .05). Our findings showed that pathogenesis of sIUGR may be related to the co-effect of the up-regulated protein expression of CDKN1C and down-regulated mRNA expression of KCNQ1OT1 in the placenta.

scholarly journals The effects of sildenafil citrate on feto–placental development and haemodynamics in a rabbit model of intrauterine growth restriction

2017 ◽  
Vol 29 (6) ◽  
pp. 1239 ◽  
Author(s):  
Jorge López-Tello ◽  
María Arias-Álvarez ◽  
Maria-Ángeles Jiménez-Martínez ◽  
Alicia Barbero-Fernández ◽  
Rosa María García-García ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Intrauterine Growth Restriction ◽  
Rabbit Model ◽  
Growth Restriction ◽  
Sildenafil Citrate ◽  
Placental Development ◽  
Negative Effects ◽  
Intrauterine Growth ◽  
Potential Benefits ◽  
The Brain

The present study evaluated the effectiveness of sildenafil citrate (SC) to improve placental and fetal growth in a diet-induced rabbit model of intrauterine growth restriction (IUGR). Pregnant rabbits were fed either ad libitum (Group C) or restricted to 50% of dietary requirements (Group R) or restricted and treated with SC (Group SC). The treatment with SC improved placental development by increasing vascularity and vessel hypertrophy in the decidua. The assessment of feto–placental haemodynamics showed higher resistance and pulsatility indices at the middle cerebral artery (MCA) in fetuses treated with SC when compared with Group R, which had increased systolic peak and time-averaged mean velocities at the MCA. Furthermore, fetuses in the SC group had significantly higher biparietal and thoracic diameters and longer crown–rump lengths than fetuses in Group R. Hence, the SC group had a reduced IUGR rate and a higher kit size at birth compared with Group R. In conclusion, SC may provide potential benefits in pregnancies with placental insufficiency and IUGR, partially counteracting the negative effects of food restriction on placental development and fetal growth. However, the present study also found evidence of a possible blood overflow in the brain that warrants further investigation.

scholarly journals Placenta Transcriptome Profiling in Intrauterine Growth Restriction (IUGR)

2019 ◽  
Vol 20 (6) ◽  
pp. 1510 ◽  
Author(s):  
Marta Majewska ◽  
Aleksandra Lipka ◽  
Lukasz Paukszto ◽  
Jan Jastrzebski ◽  
Karol Szeszko ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Active Regions ◽  
Transcriptome Profiling ◽  
Growth Restriction ◽  
Functional Enrichment ◽  
Placental Development ◽  
Protein Coding ◽  
Intrauterine Growth ◽  
Intergenic Regions ◽  
Complicated Pregnancy

Intrauterine growth restriction (IUGR) is a serious pathological complication associated with compromised fetal development during pregnancy. The aim of the study was to broaden knowledge about the transcriptomic complexity of the human placenta by identifying genes potentially involved in IUGR pathophysiology. RNA-Seq data were used to profile protein-coding genes, detect alternative splicing events (AS), single nucleotide variant (SNV) calling, and RNA editing sites prediction in IUGR-affected placental transcriptome. The applied methodology enabled detection of 37,501 transcriptionally active regions and the selection of 28 differentially-expressed genes (DEGs), among them 10 were upregulated and 18 downregulated in IUGR-affected placentas. Functional enrichment annotation indicated that most of the DEGs were implicated in the processes of inflammation and immune disorders related to IUGR and preeclampsia. Additionally, we revealed that some genes (S100A13, GPR126, CTRP1, and TFPI) involved in the alternation of splicing events were mainly implicated in angiogenic-related processes. Significant SNVs were overlapped with 6533 transcripts and assigned to 2386 coding sequence (CDS), 1528 introns, 345 5’ untranslated region (UTR), 1260 3’UTR, 918 non-coding RNA (ncRNA), and 10 intergenic regions. Within CDS regions, 543 missense substitutions with functional effects were recognized. Two known mutations (rs4575, synonymous; rs3817, on the downstream region) were detected within the range of AS and DEG candidates: PA28β and PINLYP, respectively. Novel genes that are dysregulated in IUGR were detected in the current research. Investigating genes underlying the IUGR is crucial for identification of mechanisms regulating placental development during a complicated pregnancy.

scholarly journals Paternal knockout of Slc38a4/SNAT4 causes placental hypoplasia associated with intrauterine growth restriction in mice

2019 ◽  
Vol 116 (42) ◽  
pp. 21047-21053 ◽  
Author(s):  
Shogo Matoba ◽  
Shoko Nakamuta ◽  
Kento Miura ◽  
Michiko Hirose ◽  
Hirosuke Shiura ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Embryonic Development ◽  
Intrauterine Growth Restriction ◽  
Molecular Mechanisms ◽  
Growth Restriction ◽  
Metabolome Analysis ◽  
Placental Development ◽  
Short Side ◽  
Intrauterine Growth

The placenta is critical in mammalian embryonic development because the embryo’s supply of nutrients, including amino acids, depends solely on mother-to-embryo transport through it. However, the molecular mechanisms underlying this amino acid supply are poorly understood. In this study, we focused on system A amino acid transporters Slc38a1/SNAT1, Slc38a2/SNAT2, and Slc38a4/SNAT4, which carry neutral, short-side-chain amino acids, to determine their involvement in placental or embryonic development. A triple-target CRISPR screen identified Slc38a4/SNAT4 as the critical amino acid transporter for placental development in mice. We established mouse lines from the CRISPR founders with large deletions in Slc38a4 and found that, consistent with the imprinted paternal expression of Slc38a4/SNAT4 in the placenta, paternal knockout (KO) but not maternal KO of Slc38a4/SNAT4 caused placental hypoplasia associated with reduced fetal weight. Immunostaining revealed that SNAT4 was widely expressed in differentiating cytotrophoblasts and maturing trophoblasts at the maternal–fetal interface. A blood metabolome analysis revealed that amino acid concentrations were globally reduced in Slc38a4/SNAT4 mutant embryos. These results indicated that SNAT4-mediated amino acid transport in mice plays a major role in placental and embryonic development. Given that expression of Slc38a4 in the placenta is conserved in other species, our Slc38a4/SNAT4 mutant mice could be a promising model for the analysis of placental defects leading to intrauterine growth restriction in mammals.

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