scholarly journals Alteration of placental haemostatic mechanisms in idiopathic intrauterine growth restriction

2012 ◽  
Vol 17 (2) ◽  
pp. 179 ◽  
Author(s):  
Reggie García-Robles ◽  
Paola Andrea Ayala-Ramírez ◽  
Alejandra Espinosa ◽  
Mercedes Olaya ◽  
Juan Diego Rojas ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Intrauterine Growth Restriction ◽  
Placental Tissue ◽  
Growth Restriction ◽  
Abnormal Development ◽  
Histological Evaluation ◽  
Mrna Levels ◽  
Perinatal Morbidity ◽  
Intrauterine Growth ◽  
Coagulation Abnormalities

Intrauterine growth restriction is a complication of pregnancy with a high probability of perinatal morbidity and mortality. It appears to be caused by abnormal development of placental vasculature. Haemostatic processes are important for the development of the placenta, and an imbalance between procoagulant and anticoagulant factors has been associated with risk of intrauterine growth restriction.<strong> Objective</strong>. To evaluate coagulation abnormalities in placenta of pregnancies complicated with idiopathic intrauterine growth restriction. <strong>Materials and methods</strong>. Five placentas from pregnancies with idiopathic intrauterine growth restriction were compared to 19 controls. We performed gross and histological examination of the placenta. Analysis was made of both mRNA expression by real-time PCR<br />and protein by ELISA of tissue factor and thrombomodulin in placental tissue. <strong>Results</strong>. Results based on histological evaluation were consistent with an increased prothrombotic state in placentas from pregnancies with idiopathic intrauterine growth restriction, and thrombosis of chorionic vessels was the most important finding. The study showed an increased expression of tissue factor protein (p=0.0411) and an increase in the ratio of tissue factor/thrombomodulin mRNA (p=0.0411) and protein (p=0.0215) in placentas from pregnancies with idiopathic intrauterine growth restriction. There were no statistically significant differences neither between cases and controls in the mRNA levels of tissue factor or thrombomodulin nor at the protein level of thrombomodulin. <strong>Conclusion</strong>. Evidence of alteration of local haemostatic mechanisms at the level of the placenta, including abnormal expression of tissue factor and tissue factor/thrombomodulin ratio, in pregnancies that occur with idiopathic intrauterine growth restriction is presented.<br /><strong>Key words</strong>: intrautherine growth restriction, tissue factor, thrombomodulin, placenta diseases.

Placental mitochondrial content and function in intrauterine growth restriction and preeclampsia

2014 ◽  
Vol 306 (4) ◽  
pp. E404-E413 ◽  
Author(s):  
C. Mandò ◽  
C. De Palma ◽  
T. Stampalija ◽  
G. M. Anelli ◽  
M. Figus ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Intrauterine Growth Restriction ◽  
Placental Tissue ◽  
Growth Restriction ◽  
Elective Cesarean Section ◽  
Mrna Levels ◽  
Respiratory Chain Complexes ◽  
Mitochondrial Content ◽  
Intrauterine Growth ◽  
Cytotrophoblast Cells

Intrauterine growth restriction (IUGR) and pregnancy hypertensive disorders such as preeclampsia (PE) associated with IUGR share a common placental phenotype called “placental insufficiency”, originating in early gestation when high availability of energy is required. Here, we assess mitochondrial content and the expression and activity of respiratory chain complexes (RCC) in placental cells of these pathologies. We measured mitochondrial (mt)DNA and nuclear respiratory factor 1 ( NRF1) expression in placental tissue and cytotrophoblast cells, gene and protein expressions of RCC (real-time PCR and Western blotting) and their oxygen consumption, using the innovative technique of high-resolution respirometry. We analyzed eight IUGR, six PE, and eight uncomplicated human pregnancies delivered by elective cesarean section. We found lower mRNA levels of complex II, III, and IV in IUGR cytotrophoblast cells but no differences at the protein level, suggesting a posttranscriptional compensatory regulation. mtDNA was increased in IUGR placentas. Both mtDNA and NRF1 expression were instead significantly lower in their isolated cytotrophoblast cells. Finally, cytotrophoblast RCC activity was significantly increased in placentas of IUGR fetuses. No significant differences were found in PE placentas. This study provides genuine new data into the complex physiology of placental oxygenation in IUGR fetuses. The higher mitochondrial content in IUGR placental tissue is reversed in cytotrophoblast cells, which instead present higher mitochondrial functionality. This suggests different mitochondrial content and activity depending on the placental cell lineage. Increased placental oxygen consumption might represent a limiting step in fetal growth restriction, preventing adequate oxygen delivery to the fetus.

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

Differential regulation of igf1 and igf1r mRNA levels in the two hepatic lobes following intrauterine growth restriction and its treatment with intra-amniotic insulin-like growth factor-1 in ovine fetuses

2010 ◽  
Vol 22 (8) ◽  
pp. 1188 ◽  
Author(s):  
Revati A. Darp ◽  
Hendrina A. de Boo ◽  
Hui Hui Phua ◽  
Mark H. Oliver ◽  
José G. B. Derraik ◽  
...  
Keyword(s):  
Growth Factor ◽  
Intrauterine Growth Restriction ◽  
Venous Blood ◽  
Growth Restriction ◽  
Mrna Levels ◽  
Insulin Like Growth Factor ◽  
Hepatic Lobe ◽  
Intrauterine Growth ◽  
The Right ◽  
Gut Maturation

Intrauterine growth restriction (IUGR) has life-long health implications, yet there is no effective prenatal treatment. Daily intra-amniotic administration of insulin-like growth factor (IGF)-1 to IUGR fetal sheep improves fetal gut maturation but suppresses hepatic igf1 gene expression. Fetal hepatic blood supply is regulated, in part, by shunting of oxygen- and nutrient-rich umbilical venous blood through the ductus venosus, with the left hepatic lobe predominantly supplied by umbilical venous blood and the right hepatic lobe predominantly supplied by the portal circulation. We hypothesised that: (1) once-weekly intra-amniotic IGF-1 treatment of IUGR would be effective in promoting gut maturation; and (2) IUGR and its treatment with intra-amniotic IGF-1 would differentially affect igf1 and igf1r mRNA expression in the two hepatic lobes. IUGR fetuses received 360 µg IGF-1 or saline intra-amniotically once weekly from 110 until 131 days gestation. Treatment of IUGR fetuses with IGF-1 reversed impaired gut growth. In unembolised, untreated control fetuses, igf1 mRNA levels were 19% lower in the right hepatic lobe than in the left; in IUGR fetuses, igf1 and igf1r mRNA levels were sixfold higher in the right lobe. IGF-1 treatment reduced igf1 and igf1r mRNA levels in both lobes compared with IUGR fetuses. Thus, weekly intra-amniotic IGF-1 treatment, a clinically feasible approach, reverses the impaired gut development seen in IUGR. Furthermore, igf1 and igf1r mRNA levels are differentially expressed in the two hepatic lobes and relative expression in the two lobes is altered by both IUGR and intra-amniotic IGF-1 treatment.

scholarly journals Reduced Placental 11β-Hydroxysteroid Dehydrogenase Type 2 mRNA Levels in Human Pregnancies Complicated by Intrauterine Growth Restriction: An Analysis of Possible Mechanisms

2001 ◽  
Vol 86 (10) ◽  
pp. 4979-4983 ◽  
Author(s):  
C. L. McTernan ◽  
N. Draper ◽  
H. Nicholson ◽  
S. M. Chalder ◽  
P. Driver ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Intrauterine Growth Restriction ◽  
Subsequent Development ◽  
Hydroxysteroid Dehydrogenase ◽  
Underlying Mechanism ◽  
Growth Restriction ◽  
Mrna Levels ◽  
Intrauterine Growth ◽  
Apparent Mineralocorticoid Excess

11β-Hydroxysteroid dehydrogenase type 2 (11β-HSD2) inactivates cortisol to cortisone. In the placenta 11β-HSD2 activity is thought to protect the fetus from the deleterious effects of maternal glucocorticoids. Patients with apparent mineralocorticoid excess owing to mutations in the 11β-HSD2 gene invariably have reduced birth weight, and we have recently shown reduced placental 11β-HSD2 activity in pregnancies complicated by intrauterine growth restriction. This is reflected in the literature by evidence of hypercortisolemia in the fetal circulation of small babies. In this study we have determined the levels of placental 11β-HSD2 mRNA expression across normal gestation (n = 86 placentae) and in pregnancies complicated by intrauterine growth restriction (n = 19) and evaluated the underlying mechanism for any aberrant 11β-HSD2 mRNA expression in intrauterine growth restriction. 11β-HSD2 mRNA expression increased more than 50-fold across gestation, peaking at term. Placental 11β-HSD2 mRNA levels were significantly decreased in intrauterine growth restriction pregnancies when compared with gestationally matched, appropriately grown placentae [e.g. at termΔ Ct (11β-hydroxysteroid dehydrogenase type 2/18S) 12.8 ± 0.8 (mean ± se) vs. 10.2 ± 0.2, respectively, P &lt; 0.001]. These differences were not attributable to changes in trophoblast mass in intrauterine growth restriction placentae, as assessed by parallel analyses of cytokeratin-8 mRNA expression. No mutations were found in the 11β-HSD2 gene in the intrauterine growth restriction cohort, and imprinting analysis revealed that the 11β-HSD2 gene was not imprinted. Although the underlying cause is unknown, 11β-HSD2 gene expression is reduced in intrauterine growth restriction pregnancies. These data highlight the important role of 11β-HSD2 in regulating fetal growth, a known factor in determining fetal morbidity but also the subsequent development of cardiovascular disease in adulthood.

Experimental aspects of nutrition and fetal growth

1998 ◽  
Vol 10 (2) ◽  
pp. 91-107 ◽  
Author(s):  
FH Bloomfield ◽  
JE Harding
Keyword(s):  
Effective Treatment ◽  
Fetal Growth ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Perinatal Morbidity ◽  
Intrauterine Growth ◽  
Fetal Nutrition ◽  
Determining Factor ◽  
Ultrasound Evidence ◽  
Made In

Intrauterine growth restriction (IUGR) remains a major cause of perinatal morbidity and mortality and, as yet, there is no effective treatment. Most fetuses with ultrasound evidence of moderate to severe IUGR do not grow better out of the womb than in, despite early enteral feeds and subsequent calorie supplementation. Research into possible therapies for growth restricted babies has thus also been directed towards the fetus. Major advances have been made in recent years in the understanding of the physiology of fetal growth, and it has become clear that fetal nutrition is the determining factor.

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.

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