Effect of Placental Tissue Sampling Site on Placental Protein Expression Outcome

Abstract Background Antenatal depression affects 10–20% of pregnant women. Around 2–4% of European pregnant women use antidepressant treatment, most commonly selective serotonin reuptake inhibitors (SSRIs). Poor pregnancy outcomes, such as preterm birth and low birth weight, have been described in women with antenatal depression and in pregnant women on SSRI treatment. However, the effects of antenatal depression and antidepressant treatment on the placenta are largely unknown. The aim of this work was to compare placental gene and protein expression in healthy women, women with untreated antenatal depression and women on antidepressant treatment during pregnancy. Methods Placental samples from 47 controls, 25 depressed and 45 SSRI-treated women were analysed by means of qPCR using custom-designed TaqMan low-density arrays (TLDAs) for 44 genes previously known to be involved in the pathophysiology of depression, and expressed in the placenta. Moreover, placental protein expression was determined by means of immunohistochemistry in 37 healthy controls, 13 women with untreated depression and 21 women on antidepressant treatment. Statistical comparisons between groups were performed by one-way ANOVA or the Kruskal–Wallis test. Results Nominally significant findings were noted for HTR1A and NPY2R, where women with untreated depression displayed higher gene expression than healthy controls (p < 0.05), whereas women on antidepressant treatment had similar expression as healthy controls. The protein expression analyses revealed higher expression of HTR1A in placentas from women on antidepressant treatment, than in placentas from healthy controls (p < 0.05). Conclusion The differentially expressed HTR1A, both at the gene and the protein level that was revealed in this study, suggests the involvement of HTR1A in the effect of antenatal depression on biological mechanisms in the placenta. More research is needed to elucidate the role of depression and antidepressant treatment on the placenta, and, further, the effect on the fetus.

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

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1604956.1098054 ◽

2010 ◽

Author(s):

Sue Malcolm ◽

Sayeda Abu-Amero

Keyword(s):

Gene Expression ◽

Intrauterine Growth Restriction ◽

Sampling Site ◽

Placental Tissue ◽

Growth Restriction ◽

Intrauterine Growth

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Influence of maternal lipid profile on placental protein expression of LDLr and SR-BI

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2007.05.002 ◽

2007 ◽

Vol 359 (1) ◽

pp. 8-14 ◽

Cited By ~ 35

Author(s):

M. Ethier-Chiasson ◽

A. Duchesne ◽

J.-C. Forest ◽

Y. Giguère ◽

A. Masse ◽

...

Keyword(s):

Protein Expression ◽

Lipid Profile ◽

Placental Protein

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

Placenta ◽

10.1016/j.placenta.2009.12.002 ◽

2010 ◽

Vol 31 (3) ◽

pp. 178-185 ◽

Cited By ~ 30

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

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Placental expression of proteases and their inhibitors in patients with HELLP syndrome

Biological Chemistry ◽

10.1515/bc.2009.123 ◽

2009 ◽

Vol 390 (11) ◽

Cited By ~ 5

Author(s):

Stephanie Pildner von Steinburg ◽

Achim Krüger ◽

Thorsten Fischer ◽

Karl-Theodor Mario Schneider ◽

Manfred Schmitt

Keyword(s):

Protein Expression ◽

Mrna Expression ◽

Plasminogen Activator ◽

Hellp Syndrome ◽

Mrna Level ◽

Placental Tissue ◽

Northern Blotting ◽

Trophoblast Invasion ◽

Matrix Remodeling ◽

Elevated Liver Enzymes

AbstractIn preeclampsia and hemolysis, elevated liver enzymes and low platelet (HELLP) syndrome, impaired trophoblast invasion and excessive fibrin deposition in the placental intervillous space is associated with fetal compromise. However, little information is available whether modulation of placental protease expression – potentially causing impaired trophoblast invasion – is associated with the HELLP syndrome. Total RNA and protein were extracted from placental tissue from 11 females with HELLP syndrome and 8 controls matched for gestational age. mRNA expression of matrix metalloprotease (MMP) -2 and -9, tissue inhibitors of metalloprotease (TIMP) -1, -2, and -3, and urokinase-type plasminogen activator receptor (uPAR) was determined by Northern blotting. Protein expression of MMP-2 and -9, and TIMP-1 and -2 was detected by Western blotting and that of uPA, uPAR, and plasminogen activator inhibitor (PAI) -1 by ELISA. In patients with HELLP syndrome, mRNA expression of MMP-2 and TIMP-2 was decreased, whereas TIMP-1 and -3 levels were unchanged. MMP-9 and uPAR mRNA was undetectable in both groups. Protein expression of all investigated proteolytic factors remained unchanged. Our findings at the mRNA level suggest a decrease in matrix remodeling in placentae from patients with HELLP syndrome compared with control pregnancies, although this is not supported at the protein level.

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Expression of genes involved in inflammation and growth – does sampling site in human full-term placenta matter?

Journal of Perinatal Medicine ◽

10.1515/jpm-2018-0290 ◽

2019 ◽

Vol 47 (5) ◽

pp. 539-546

Author(s):

Marianne Allbrand ◽

Jan Åman ◽

Kerstin Nilsson ◽

Yang Cao ◽

Maria Lodefalk

Keyword(s):

Gene Expression ◽

Growth Factor ◽

Hepatocyte Growth Factor ◽

Sampling Site ◽

Growth Factor Receptor ◽

Placental Tissue ◽

Normal Weight ◽

Full Term ◽

Singleton Pregnancy ◽

Hepatocyte Growth

Abstract Objective To investigate the placental gene expression of substances in the inflammatory cascade and growth factors at nine different well-defined sampling sites in full-term placentas from 12 normal weight healthy non-smoking women with an uncomplicated singleton pregnancy. Methods All placentas (six girls and six boys) were delivered vaginally. Quantitative real-time polymerase chain reaction was used to analyze toll receptor-2 and -4, interleukin-6 and -8, tumor necrosis factor-α, leptin, ghrelin, insulin-like growth factor-1 and -2, hepatocyte growth factor, hepatocyte growth factor receptor and insulin receptor (IR). Results The leptin gene and the IR gene showed higher expression in lateral regions near the chorionic plate compared to central regions near the basal plate (P = 0.028 and P = 0.041, respectively). Conclusion Our results suggest that the sampling site may influence the gene expression for leptin and IR in placental tissue obtained from full-term normal pregnancies. We speculate that this may be due to differences in placental structure and perfusion and may be important when future studies are designed.

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Modulation of placental protein expression of OLR1: implication in pregnancy-related disorders or pathologies

Reproduction ◽

10.1530/rep-08-0082 ◽

2008 ◽

Vol 136 (4) ◽

pp. 491-502 ◽

Cited By ~ 16

Author(s):

M Ethier-Chiasson ◽

J-C Forest ◽

Y Giguère ◽

A Masse ◽

C Marseille-Tremblay ◽

...

Keyword(s):

Protein Expression ◽

Lipid Profile ◽

Total Cholesterol ◽

Cholesterol Level ◽

Plasma Cholesterol ◽

Total Cholesterol Level ◽

Low Density Lipoprotein ◽

Ldl Receptor ◽

Density Lipoprotein ◽

Placental Protein

The lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (OLR1) is a newly described receptor for oxidatively modified LDL. The human pregnancy is associated with hyperlipidemia and oxidative stress. It has been reported that modification in maternal lipid profile can induce disturbance during pregnancy. In this study, we have evaluated the expression protein level of OLR1 in human term placenta of women having plasma cholesterol level lower to 7 mM or higher to 8 mM and women of gestational diabetes mellitus (GDM) by western blot analysis. The present study demonstrates that the maternal lipid profile is associated with placental protein expression of OLR1. A significant increase in the protein expression of OLR1 was observed in placenta of women with elevated plasmatic total cholesterol level (>8 mM). In addition, the placental protein expression of OLR1 is increased in mothers having the highest pre-pregnancy body mass index (BMI) and low (<7 mM) plasmatic total cholesterol level at term. Interestingly, the placental protein expression of OLR1 is increased in the presence of GDM pregnancies compared with normal lipids level pregnancies, without the modification of mRNA expression. In conclusion, placental OLR1 protein expression is associated with maternal lipid profile, pre-pregnancy BMI, and pathology of GDM.

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Calcifediol Decreases Interleukin-6 Secretion by Cultured Human Trophoblasts From GDM Pregnancies

Journal of the Endocrine Society ◽

10.1210/js.2019-00181 ◽

2019 ◽

Vol 3 (11) ◽

pp. 2165-2178 ◽

Cited By ~ 2

Author(s):

Marilyn Lacroix ◽

Farah Lizotte ◽

Marie-France Hivert ◽

Pedro Geraldes ◽

Patrice Perron

Keyword(s):

Vitamin D ◽

Placental Tissue ◽

Target Cells ◽

Compensatory Mechanism ◽

Tissue Samples ◽

Diet And Exercise ◽

Protein Expressions ◽

Placental Protein ◽

Nongenomic Effects ◽

Inflammatory Effect

Abstract Gestational diabetes mellitus (GDM) is often characterized by low maternal calcifediol (25OHD) and high inflammation levels. This study aimed to determine whether placental protein expressions of CYP27B1, vitamin D receptor (VDR), and CYP24A1 are impaired in GDM and to investigate the effect of a 25OHD treatment on IL-6 secretion by GDM trophoblasts compared with normoglycemic (NG) trophoblasts. Placental tissue samples were harvested to determine protein expression of CYP27B1, VDR, and CYP24A1 by immunoblots. Isolated trophoblasts were stimulated with 25OHD concentrations (25 to 2000 nM) once a day for 3 days and IL-6 secretion was quantified (ELISA). We recruited 17 NG women, 19 women with GDM treated with diet and exercise alone (GDM-d) and 9 women with GDM who necessitated insulin therapy (GDM-i). Protein expressions of CYP27B1 and VDR were significantly higher in placental tissue from GDM-d women compared with NG women (both P = 0.02), whereas no differences were detected between GDM-i and NG placental tissues. In cultured trophoblasts (two groups; n = 5 NG and n = 5 GDM-d), exposure to increasing 25OHD concentrations significantly decreased IL-6 secretion in the GDM-d group only (P = 0.006). After treatment with 25OHD (2000 nM), IL-6 secretion was lower in the GDM-d group compared with the NG group (P = 0.03). Our results suggest an upregulation of the VDR-1,25(OH)2D complex bioavailability in GDM-d placentas, possibly reflecting a compensatory mechanism aiming to ensure that vitamin D can exert its genomic and nongenomic effects in the target cells of the placental-fetal unit. Our findings support an anti-inflammatory effect of vitamin D at the feto-maternal interface in GDM-d pregnancies.

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Direct Involvement of HERV-W Env Glycoprotein in Human Trophoblast Cell Fusion and Differentiation

Molecular and Cellular Biology ◽

10.1128/mcb.23.10.3566-3574.2003 ◽

2003 ◽

Vol 23 (10) ◽

pp. 3566-3574 ◽

Cited By ~ 286

Author(s):

Jean-Louis Frendo ◽

Delphine Olivier ◽

Valérie Cheynet ◽

Jean-Luc Blond ◽

Olivier Bouton ◽

...

Keyword(s):

Protein Expression ◽

Cell Fusion ◽

Primary Cultures ◽

Placental Tissue ◽

Trophoblast Cell ◽

Direct Role ◽

Human Trophoblast ◽

Type D ◽

Env Protein

ABSTRACT We recently demonstrated that the product of the HERV-W env gene, a retroviral envelope protein also dubbed syncytin, is a highly fusogenic membrane glycoprotein inducing the formation of syncytia on interaction with the type D mammalian retrovirus receptor. In addition, the detection of HERV-W Env protein (Env-W) expression in placental tissue sections led us to propose a role for this fusogenic glycoprotein in placenta formation. To evaluate this hypothesis, we analyzed the involvement of Env-W in the differentiation of primary cultures of human villous cytotrophoblasts that spontaneously differentiate by cell fusion into syncytiotrophoblasts in vitro. First, we observed that HERV-W env mRNA and glycoprotein expression are colinear with primary cytotrophoblast differentiation and with expression of human chorionic gonadotropin (hCG), a marker of syncytiotrophoblast formation. Second, we observed that in vitro stimulation of trophoblast cell fusion and differentiation by cyclic AMP is also associated with a concomitant increase in HERV-W env and hCG mRNA and protein expression. Finally, by using specific antisense oligonucleotides, we demonstrated that inhibition of Env-W protein expression leads to a decrease of trophoblast fusion and differentiation, with the secretion of hCG in culture medium of antisense oligonucleotide-treated cells being decreased by fivefold. Taken together, these results strongly support a direct role for Env-W in human trophoblast cell fusion and differentiation.

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