Normal and Pathological Placental Development: MRI and Pathology

: Obesity and gestational diabetes mellitus (GDM) are becoming more common among pregnant women worldwide and are individually associated with a number of placenta-mediated obstetric complications, including preeclampsia, macrosomia, intrauterine growth restriction and stillbirth. The placenta serves several functions throughout pregnancy and is the main exchange site for the transfer of nutrients and gas from mother to fetus. In pregnancies complicated by maternal obesity or GDM, the placenta is exposed to environmental changes, such as increased inflammation and oxidative stress, dyslipidemia, and altered hormone levels. These changes can affect placental development and function and lead to abnormal fetal growth and development as well as metabolic and cardiovascular abnormalities in the offspring. This review aims to summarize current knowledge on the effects of obesity and GDM on placental development and function. Understanding these processes is key in developing therapeutic interventions with the goal of mitigating these effects and preventing future cardiovascular and metabolic pathology in subsequent generations.

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The TGFβ Family in Human Placental Development at the Fetal-Maternal Interface

Biomolecules ◽

10.3390/biom10030453 ◽

2020 ◽

Vol 10 (3) ◽

pp. 453

Author(s):

Susana M. Chuva de Sousa Lopes ◽

Marta S. Alexdottir ◽

Gudrun Valdimarsdottir

Keyword(s):

Stem Cell ◽

Transforming Growth Factor Beta ◽

Molecular Mechanisms ◽

Transforming Growth Factor ◽

Cell Model ◽

Embryonic Stem ◽

Model Systems ◽

Special Focus ◽

Placental Development

Emerging data suggest that a trophoblast stem cell (TSC) population exists in the early human placenta. However, in vitro stem cell culture models are still in development and it remains under debate how well they reflect primary trophoblast (TB) cells. The absence of robust protocols to generate TSCs from humans has resulted in limited knowledge of the molecular mechanisms that regulate human placental development and TB lineage specification when compared to other human embryonic stem cells (hESCs). As placentation in mouse and human differ considerably, it is only with the development of human-based disease models using TSCs that we will be able to understand the various diseases caused by abnormal placentation in humans, such as preeclampsia. In this review, we summarize the knowledge on normal human placental development, the placental disease preeclampsia, and current stem cell model systems used to mimic TB differentiation. A special focus is given to the transforming growth factor-beta (TGFβ) family as it has been shown that the TGFβ family has an important role in human placental development and disease.

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323: Pravastatin improves pregnancy outcome and placental development in heme oxygenase-1 deficient mice

American Journal of Obstetrics and Gynecology ◽

10.1016/j.ajog.2017.10.259 ◽

2018 ◽

Vol 218 (1) ◽

pp. S202-S203

Author(s):

Abraham Tsur ◽

Flora Kalish ◽

Jordan Burgess ◽

Hui Zhao ◽

Kerriann Casey ◽

...

Keyword(s):

Pregnancy Outcome ◽

Heme Oxygenase ◽

Heme Oxygenase 1 ◽

Placental Development ◽

Deficient Mice

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Independent pseudogenizations and losses of sox15 during amniote diversification following asymmetric ohnolog evolution

BMC Ecology and Evolution ◽

10.1186/s12862-021-01864-z ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Yusaku Ogita ◽

Kei Tamura ◽

Shuuji Mawaribuchi ◽

Nobuhiko Takamatsu ◽

Michihiko Ito

Keyword(s):

Sequence Similarity ◽

The Other ◽

Vertebrate Evolution ◽

Skeletal Muscle Regeneration ◽

Cns Development ◽

Placental Development ◽

Relaxed Selection ◽

Significant Sequence Similarity ◽

Anuran Amphibians ◽

Divergent Gene

Abstract Background Four ohnologous genes (sox1, sox2, sox3, and sox15) were generated by two rounds of whole-genome duplication in a vertebrate ancestor. In eutherian mammals, Sox1, Sox2, and Sox3 participate in central nervous system (CNS) development. Sox15 has a function in skeletal muscle regeneration and has little functional overlap with the other three ohnologs. In contrast, the frog Xenopus laevis and zebrafish orthologs of sox15 as well as sox1-3 function in CNS development. We previously reported that Sox15 is involved in mouse placental development as neofunctionalization, but is pseudogenized in the marsupial opossum. These findings suggest that sox15 might have evolved with divergent gene fates during vertebrate evolution. However, knowledge concerning sox15 in other vertebrate lineages than therian mammals, anuran amphibians, and teleost fish is scarce. Our purpose in this study was to clarify the fate and molecular evolution of sox15 during vertebrate evolution. Results We searched for sox15 orthologs in all vertebrate classes from agnathans to mammals by significant sequence similarity and synteny analyses using vertebrate genome databases. Interestingly, sox15 was independently pseudogenized at least twice during diversification of the marsupial mammals. Moreover, we observed independent gene loss of sox15 at least twice during reptile evolution in squamates and crocodile-bird diversification. Codon-based phylogenetic tree and selective analyses revealed an increased dN/dS ratio for sox15 compared to the other three ohnologs during jawed vertebrate evolution. Conclusions The findings revealed an asymmetric evolution of sox15 among the four ohnologs during vertebrate evolution, which was supported by the increased dN/dS values in cartilaginous fishes, anuran amphibians, and amniotes. The increased dN/dS value of sox15 may have been caused mainly by relaxed selection. Notably, independent pseudogenizations and losses of sox15 were observed during marsupial and reptile evolution, respectively. Both might have been caused by strong relaxed selection. The drastic gene fates of sox15, including neofunctionalization and pseudogenizations/losses during amniote diversification, might be caused by a release from evolutionary constraints.

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X chromosome-dependent disruption of placental regulatory networks in hybrid dwarf hamsters

Genetics ◽

10.1093/genetics/iyab043 ◽

2021 ◽

Author(s):

Thomas D Brekke ◽

Emily C Moore ◽

Shane C Campbell-Staton ◽

Colin M Callahan ◽

Zachary A Cheviron ◽

...

Keyword(s):

Gene Expression ◽

X Chromosome ◽

Regulatory Networks ◽

Mammalian Species ◽

Strongly Correlated ◽

Placental Development ◽

Substitution Lines ◽

Genome Wide ◽

Highly Sensitive ◽

First And Second Generation

AbstractEmbryonic development in mammals is highly sensitive to changes in gene expression within the placenta. The placenta is also highly enriched for genes showing parent-of-origin or imprinted expression, which is predicted to evolve rapidly in response to parental conflict. However, little is known about the evolution of placental gene expression, or if divergence of placental gene expression plays an important role in mammalian speciation. We used crosses between two species of dwarf hamsters (Phodopus sungorus and Phodopus campbelli) to examine the genetic and regulatory underpinnings of severe placental overgrowth in their hybrids. Using quantitative genetic mapping and mitochondrial substitution lines, we show that overgrowth of hybrid placentas was primarily caused by genetic differences on the maternally inherited P. sungorus X chromosome. Mitochondrial interactions did not contribute to abnormal hybrid placental development, and there was only weak correspondence between placental disruption and embryonic growth. Genome-wide analyses of placental transcriptomes from the parental species and first- and second-generation hybrids revealed a central group of co-expressed X-linked and autosomal genes that were highly enriched for maternally biased expression. Expression of this gene network was strongly correlated with placental size and showed widespread misexpression dependent on epistatic interactions with X-linked hybrid incompatibilities. Collectively, our results indicate that the X chromosome is likely to play a prominent role in the evolution of placental gene expression and the accumulation of hybrid developmental barriers between mammalian species.

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Placental Transcriptome Adaptations to Maternal Nutrient Restriction in Sheep

International Journal of Molecular Sciences ◽

10.3390/ijms22147654 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7654

Author(s):

Chelsie B. Steinhauser ◽

Colleen A. Lambo ◽

Katharine Askelson ◽

Gregory W. Burns ◽

Susanta K. Behura ◽

...

Keyword(s):

Mhc Class Ii ◽

Killer Cell ◽

National Research Council ◽

Enrichment Analysis ◽

Nutrient Utilization ◽

Gene Set Enrichment Analysis ◽

Nutrient Restriction ◽

Placental Development ◽

Gene Set Enrichment ◽

Pregnant Sheep

Placental development is modified in response to maternal nutrient restriction (NR), resulting in a spectrum of fetal growth rates. Pregnant sheep carrying singleton fetuses and fed either 100% (n = 8) or 50% (NR; n = 28) of their National Research Council (NRC) recommended intake from days 35–135 of pregnancy were used to elucidate placentome transcriptome alterations at both day 70 and day 135. NR fetuses were further designated into upper (NR NonSGA; n = 7) and lower quartiles (NR SGA; n = 7) based on day 135 fetal weight. At day 70 of pregnancy, there were 22 genes dysregulated between NR SGA and 100% NRC placentomes, 27 genes between NR NonSGA and 100% NRC placentomes, and 22 genes between NR SGA and NR NonSGA placentomes. These genes mediated molecular functions such as MHC class II protein binding, signaling receptor binding, and cytokine activity. Gene set enrichment analysis (GSEA) revealed significant overrepresentation of genes for natural-killer-cell-mediated cytotoxicity in NR SGA compared to 100% NRC placentomes, and alterations in nutrient utilization pathways between NR SGA and NR NonSGA placentomes at day 70. Results identify novel factors associated with impaired function in SGA placentomes and potential for placentomes from NR NonSGA pregnancies to adapt to nutritional hardship.

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The comparison of pro- and antioxidative parameters in plasma and placental tissues during early phase of placental development in cows

Molecular Biology Reports ◽

10.1007/s11033-021-06143-0 ◽

2021 ◽

Author(s):

Jacek Wawrzykowski ◽

Monika Jamioł ◽

Wioleta Mojsym ◽

Marta Kankofer

Keyword(s):

Blood Plasma ◽

Antioxidative Enzymes ◽

Placental Development ◽

Blood Samples ◽

Bovine Placenta ◽

Total Antioxidant ◽

Tissue Homogenates ◽

Further Development ◽

General Profile ◽

In Blood Plasma

AbstractPhysiological balance between pro- and antioxidative processes is crucial for placentation and further development of fetus and placenta. Parameters of pro- and antioxidative profile may serve as markers of proper course of pregnancy. The aim of study was to assess whether the balance between pro- and antioxidative parameters during placentation phase in bovine placenta is maintained. Placental and blood samples were collected from healthy, HF, pregnant (2nd-3rd month) cows (n = 8) in slaughterhouse and in farm, respectively. Formylokinurenine and bityrosine content were measured spectrofluorimetrically in blood plasma and tissue homogenates while metabolites of lipid peroxidation, total antioxidant capacity, SH groups and activity of antioxidative enzymes (glutathione peroxidase and superoxide dismutase) were determined in examined tissues by spectrophotometry. Western blotting was used to confirm the presence of enzymatic proteins in placenta. Results: Local profile in tissues was more pronounced than general profile in blood plasma. Activities of antioxidative enzymes were significantly (p < 0.05) higher in 2nd compared to 3rd month of pregnancy in maternal part of placenta while prooxidant parameters showed opposite relationship. Obtained results showed significant differences when compared to data from non-pregnant animals or time of parturition. Further studies are necessary for elucidation of placentation phase in cows.

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