scholarly journals miRNAs and Their Gene Targets—A Clue to Differentiate Pregnancies with Small for Gestational Age Newborns, Intrauterine Growth Restriction, and Preeclampsia

Diagnostics ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 729
Author(s):  
Angelika V. Timofeeva ◽  
Ivan S. Fedorov ◽  
Alexander G. Brzhozovskiy ◽  
Anna E. Bugrova ◽  
Vitaliy V. Chagovets ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Molecular Mechanisms ◽  
Clinical Manifestations ◽  
Placental Tissue ◽  
Growth Restriction ◽  
Molecular Profile ◽  
Intrauterine Growth ◽  
Protein Mass ◽  
Protein Mass Spectrometry ◽  
Gene Expression Levels

Despite the differences in the clinical manifestations of major obstetric syndromes, such as preeclampsia (PE) and intrauterine growth restriction (IUGR), their pathogenesis is based on the dysregulation of proliferation, differentiation, and invasion of cytotrophoblast cells that occur in the developing placenta, decidual endometrium, and myometrial parts of the spiral arteries. To understand the similarities and differences in the molecular mechanisms of PE and IUGR, samples of the placental bed and placental tissue were analyzed using protein mass spectrometry and the deep sequencing of small RNAs, followed by validation of the data obtained by quantitative RT-PCR in real time. A comparison of the transcriptome and proteomic profiles in the samples made it possible to conclude that the main changes in the molecular profile in IUGR occur in the placental bed, in contrast to PE, in which the majority of molecular changes occurs in the placenta. In placental bed samples, significant changes in the ratio of miRNA and its potential target gene expression levels were revealed, which were unique for IUGR (miR-30c-5p/VIM, miR-28-3p/VIM, miR-1-3p/ANXA2, miR-30c-5p/FBN1; miR-15b-5p/MYL6), unique for PE (miR-185-3p/FLNA), common for IUGR and PE (miR-30c-5p/YWHAZ and miR-654-3p/FGA), but all associated with abnormality in the hemostatic and vascular systems as well as with an inflammatory process at the fetal‒maternal interface.

scholarly journals The role of apoptosis in the complex pathogenesis of the most common obstetrics and gynaecology diseases

2020 ◽  
Vol 107 (1) ◽  
pp. 106-119
Author(s):  
P. Kovács ◽  
József Gábor Joó ◽  
V. Tamás ◽  
Z. Molnár ◽  
D. Burik-Hajas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intrauterine Growth Restriction ◽  
Placental Tissue ◽  
Growth Restriction ◽  
Tissue Samples ◽  
Intrauterine Growth ◽  
Pcr Method ◽  
Bax Gene ◽  
Gene Expression Levels

AbstractPurposeWe aimed to assess the etiological role of apoptotic genes Bcl-2 and Bax in the background of major obstetric and gynaecological diseases.MethodsPlacental tissue samples were collected from 101 pregnancies with intrauterine growth restriction and 104 pregnancies with premature birth with 140 controll samples from term, eutrophic newborns. In addition, gene expression assessment of the genes Bax and Bcl-2 was performed in 101 uterine leiomyoma tissue samples at our disposal with 110 control cases. Gene expression levels were assessed by PCR method.ResultsThe expression of the Bcl-2 gene was decreased in placental samples with intrauterine growth restriction. Significant overexpression of the proapoptotic Bax gene was detected in samples from premature infants. Antiapoptotic Bcl-2 gene expression was found to be significantly increased in fibroid tissues.ConclusionApoptosis plays a crucial role in the development of the most common OB/GYN conditions. Decrease in the placental expression of the antiapoptotic gene Bcl-2 may upset the balance of programmed cell death.

Differences in gene expression dependent on sampling site in placental tissue of fetuses with intrauterine growth restriction

Placenta ◽  
2010 ◽  
Vol 31 (3) ◽  
pp. 178-185 ◽  
Author(s):  
A.A. Tzschoppe ◽  
E. Struwe ◽  
H.G. Dörr ◽  
T.W. Goecke ◽  
M.W. Beckmann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intrauterine Growth Restriction ◽  
Sampling Site ◽  
Placental Tissue ◽  
Growth Restriction ◽  
Intrauterine Growth

Microarray analysis of placental tissue in intrauterine growth restriction

2010 ◽  
Vol 72 (2) ◽  
pp. 241-247 ◽  
Author(s):  
E. Struwe ◽  
G. Berzl ◽  
R. Schild ◽  
H. Blessing ◽  
L. Drexel ◽  
...  
Keyword(s):  
Microarray Analysis ◽  
Intrauterine Growth Restriction ◽  
Placental Tissue ◽  
Growth Restriction ◽  
Intrauterine Growth

scholarly journals Human Cytomegalovirus Infection Interferes with the Maintenance and Differentiation of Trophoblast Progenitor Cells of the Human Placenta

2015 ◽  
Vol 89 (9) ◽  
pp. 5134-5147 ◽  
Author(s):  
Takako Tabata ◽  
Matthew Petitt ◽  
Martin Zydek ◽  
June Fang-Hoover ◽  
Nicholas Larocque ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Human Cytomegalovirus ◽  
Intrauterine Growth Restriction ◽  
Molecular Mechanisms ◽  
Hcmv Infection ◽  
Congenital Infection ◽  
Growth Restriction ◽  
Chorionic Villi ◽  
Intrauterine Growth

ABSTRACTHuman cytomegalovirus (HCMV) is a major cause of birth defects that include severe neurological deficits, hearing and vision loss, and intrauterine growth restriction. Viral infection of the placenta leads to development of avascular villi, edema, and hypoxia associated with symptomatic congenital infection. Studies of primary cytotrophoblasts (CTBs) revealed that HCMV infection impedes terminal stages of differentiation and invasion by various molecular mechanisms. We recently discovered that HCMV arrests earlier stages involving development of human trophoblast progenitor cells (TBPCs), which give rise to the mature cell types of chorionic villi—syncytiotrophoblasts on the surfaces of floating villi and invasive CTBs that remodel the uterine vasculature. Here, we show that viral proteins are present in TBPCs of the chorion in cases of symptomatic congenital infection.In vitrostudies revealed that HCMV replicates in continuously self-renewing TBPC lines derived from the chorion and alters expression and subcellular localization of proteins required for cell cycle progression, pluripotency, and early differentiation. In addition, treatment with a human monoclonal antibody to HCMV glycoprotein B rescues differentiation capacity, and thus, TBPCs have potential utility for evaluation of the efficacies of novel antiviral antibodies in protecting and restoring placental development. Our results suggest that HCMV replicates in TBPCs in the chorionin vivo, interfering with the earliest steps in the growth of new villi, contributing to virus transmission and impairing compensatory development. In cases of congenital infection, reduced responsiveness of the placenta to hypoxia limits the transport of substances from maternal blood and contributes to fetal growth restriction.IMPORTANCEHuman cytomegalovirus (HCMV) is a leading cause of birth defects in the United States. Congenital infection can result in permanent neurological defects, mental retardation, hearing loss, visual impairment, and pregnancy complications, including intrauterine growth restriction, preterm delivery, and stillbirth. Currently, there is neither a vaccine nor any approved treatment for congenital HCMV infection during gestation. The molecular mechanisms underlying structural deficiencies in the placenta that undermine fetal development are poorly understood. Here we report that HCMV replicates in trophoblast progenitor cells (TBPCs)—precursors of the mature placental cells, syncytiotrophoblasts and cytotrophoblasts, in chorionic villi—in clinical cases of congenital infection. Virus replication in TBPCsin vitrodysregulates key proteins required for self-renewal and differentiation and inhibits normal division and development into mature placental cells. Our findings provide insights into the underlying molecular mechanisms by which HCMV replication interferes with placental maturation and transport functions.

Postnatal development of skeletal muscle in pigs with intrauterine growth restriction: morphofunctional phenotype and molecular mechanisms

2020 ◽  
Vol 236 (5) ◽  
pp. 840-853 ◽  
Author(s):  
Fernando Felicioni ◽  
Andreia D. Pereira ◽  
Andre L. Caldeira‐Brant ◽  
Thais G. Santos ◽  
Thais M. D. Paula ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Postnatal Development ◽  
Intrauterine Growth Restriction ◽  
Molecular Mechanisms ◽  
Growth Restriction ◽  
Intrauterine Growth

Intrauterine Growth Restriction Alters the Postnatal Development of the Rat Cerebellum

2017 ◽  
Vol 39 (1-4) ◽  
pp. 215-227 ◽  
Author(s):  
Annie R.A. McDougall ◽  
Vanny Wiradjaja ◽  
Aminath Azhan ◽  
Anqi Li ◽  
Nadia Hale ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Molecular Mechanisms ◽  
Growth Restriction ◽  
Cerebellar Development ◽  
Mrna Levels ◽  
Fiber Density ◽  
Pregnant Rats ◽  
Intrauterine Growth ◽  
Protein Levels ◽  
Proliferative Zone

Intrauterine growth restriction (IUGR) is a major cause of antenatal brain injury. We aimed to characterize cerebellar deficits following IUGR and to investigate the potential underlying cellular and molecular mechanisms. At embryonic day 18, pregnant rats underwent either sham surgery (controls; n = 23) or bilateral uterine vessel ligation to restrict blood flow to fetuses (IUGR; n = 20). Offspring were collected at postnatal day 2 (P2), P7, and P35. Body weights were reduced at P2, P7, and P35 in IUGR offspring (p < 0.05) compared with controls. At P7, the width of the external granule layer (EGL) was 30% greater in IUGR than control rats (p < 0.05); there was no difference in the width of the proliferative zone or in the density of Ki67-positive cells in the EGL. Bergmann glia were disorganized at P7 and P35 in IUGR pups, and by P35, there was a 10% decrease in Bergmann glial fiber density (p < 0.05) compared with controls. At P7, trophoblast antigen-2 (Trop2) mRNA and protein levels in the cerebellum were decreased by 88 and 40%, respectively, and astrotactin 1 mRNA levels were increased by 20% in the IUGR rats (p < 0.05) compared with controls; there was no difference in ASTN1 protein. The expressions of other factors known to regulate cerebellar development (astrotactin 2, brain-derived neurotrophic factor, erb-b2 receptor tyrosine kinase 4, neuregulin 1, sonic hedgehog and somatostatin) were not different between IUGR and control rats at P7 or P35. These data suggest that damage to the migratory scaffold (Bergmann glial fibers) and alterations in the genes that influence migration (Trop2 and Astn1) may underlie the deficits in postnatal cerebellar development following IUGR.

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