Identification of Differential Gene Expression Profiles in Placentas from Preeclamptic Pregnancies Versus Normal Pregnancies by DNA Microarrays

Meng, Tao; Chen, Haiying; Sun, Manni; Wang, He; Zhao, Ge; Wang, Xiaoshuang

doi:10.1089/omi.2011.0066

Cited by 69 publications

(38 citation statements)

References 39 publications

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“…These results suggest decreased tolerogenic activity of pMw during CA. This finding may be related to the increased expression of WNT pathway genes, which are associated with inflammatory responses, and a recent study reported aberrant regulation of the WNT pathway at the transcriptional level during preeclampsia (58). Importantly, we found that pMw from CA patients were unable to mature in MGCs but that supernatant from cultured control trophoblasts was able to partially restore the ability of pMw to differentiate into MGCs.…”

Section: Discussionsupporting

confidence: 50%

Placental Macrophages Are Impaired in Chorioamnionitis, an Infectious Pathology of the Placenta

Amara

Gorvel

Baulan

et al. 2013

The Journal of Immunology

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Pregnancy is dependent on maternal–fetal tolerance that may be compromised because of infections or inflammation of the placenta. In this study, we examined whether the context of placental immune tolerance affected the functions of resident macrophages and if their functions were altered during chorioamnionitis, an infectious pathology of the placenta. Macrophages from at-term placentas expressed CD14, exhibited macrophage microbicidal functions, but were less inflammatory than monocyte-derived macrophages. Moreover, placental macrophages spontaneously matured into multinucleated giant cells (MGCs), a property not exhibited by monocyte-derived macrophages, and we detected MGCs of myeloid origin in placental tissue. Compared with placental macrophages, MGCs exhibited a specific phenotype and gene expression signature, consisting of increased cytoskeleton-associated gene expression along with depressed expression of inflammatory response genes. Furthermore, placental macrophages from patients with chorioamnionitis were unable to form MGCs, but this defect was partially corrected by incubating these placental macrophages with control trophoblast supernatants. MGCs formation likely serves to regulate their inflammatory and cytocidal activities in a context that imposes semiallograft acceptance and defense against pathogens.

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Section: Discussionsupporting

confidence: 50%

Placental Macrophages Are Impaired in Chorioamnionitis, an Infectious Pathology of the Placenta

Amara

Gorvel

Baulan

et al. 2013

The Journal of Immunology

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“…As a first step toward class discovery of PE pathology, we performed an aggregated analysis of 7 previously published human PE placental microarray data sets 4,5,[28][29][30][31][32] using unbiased/ unsupervised multivariate clustering techniques. 13 Our methods, which improve on similar approaches used for the molecular subclassification of tumors in the oncology field, 33,34 blindly group samples based solely on similarities in gene expression, independent of clinical characteristics.…”

Section: 3mentioning

confidence: 99%

“…From the Research Centre for Women's and Infants' Health BioBank, we collected 157 placenta samples (BioBank samples) with detailed clinical data from a range of hypertensive and normotensive states. To increase our sample size, the BioBank samples were then combined with the 7 previously published placental microarray data sets 4,5,[28][29][30][31][32] (Table S1 in the online-only Data Supplement) that we have previously analyzed in aggregate (Aggregate samples). 13 The final combined data set contained 330 placentas (157 PE and 173 non-PE) and expression values for 14 651 genes found in common across all original microarray platforms.…”

Section: Assembly Of the Combined Data Setmentioning

confidence: 99%

Unsupervised Placental Gene Expression Profiling Identifies Clinically Relevant Subclasses of Human Preeclampsia

et al. 2016

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P reeclampsia (PE) is a potentially life-threatening, systemic, hypertensive disorder affecting 3% to 5% of all pregnancies. Responsible for >60 000 maternal deaths each year, 1 PE is also a leading cause of fetal/neonatal mortality and morbidity. Classically, PE has been defined as new-onset hypertension and proteinuria after 20 weeks of gestation. However, the clinical presentation of PE is highly variable among women, and diagnostic guidelines now include signs and symptoms that are reflective of disease in ≥1 organ systems (liver, kidney, blood, and brain 2,3 ). Apart from expectant management and delivery of the infant and the placenta, there currently exists no cure or effective treatments for PE.The placenta is widely considered to be the central component of the PE disease process, and as it is not required after birth, this presents a unique opportunity to assess a clinically relevant tissue involved in a hypertensive pathology. Accordingly, numerous placental analyses have been conducted with the aim of identifying early detection markers or candidates for therapeutic intervention in PE. These studies have uncovered involvement of molecular pathways, such as oxidative stress and secretion, [4][5][6] and many secreted factors with disrupted expression during PE have been investigated as candidate blood biomarkers of this pathology. [7][8][9][10] However, the predictive power of these molecules demonstrate low sensitivity at clinically relevant false-positive rates 7 and, therefore, are not presently recommended for use as screening tools for PE. 11 We, [12][13][14] and others, 15,16 have proposed that this lack of robust biomarkers and effective treatments for PE is because of the multifactorial nature of this disease, a notion supported by considerable evidence within the human literature. [17][18][19][20][21] Further support also exists in the numerous developed animal models of PE that recapitulate many of the human symptoms and pathologies because these are the result of a range of initial insults, involving disruptions in placental 22,23 or maternal 24 genes, or a predisposing baseline maternal hypertension. 25 As such, past placental microarray, and even meta-analysis, 26,27 studies with small and highly selected patient cohorts, predominately assessed using a binary classification system (of PE versus control), do not accurately reflect the true clinical presentation of patients. Even the separation of women into earlyonset (diagnosis before 34 weeks) and late-onset PE groups 18,21 Abstract-Preeclampsia (PE) is a complex, hypertensive disorder of pregnancy, demonstrating considerable variability in maternal symptoms and fetal outcomes. Unfortunately, prior research has not accounted for this variability, resulting in a lack of robust biomarkers and effective treatments for PE. Here, we created a large (N=330) clinically relevant human placental microarray data set, consisting of 7 previously published studies and 157 highly annotated new samples from a single BioBank. Applying unsupervise...

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“…Several gene expression studies (Lapaire et al, 2012;Louwen et al, 2012;Meng et al, 2012;Zhou et al, 2013) have been conducted to investigate expression differences between preeclampsia patients and healthy controls. The major challenge for microarray analysis is to develop a suitable statistical model to deal with the small sample number and large number of genes.…”

Section: Introductionmentioning

confidence: 99%

Partial least squares-based gene expression analysis in preeclampsia

Jiang¹,

Yang²,

Li³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Preeclampsia is major cause of maternal and fetal morbidity and mortality. Currently, the etiology of preeclampsia is unclear. In this study, we investigated differences in gene expression between preeclampsia patients and controls using partial least squaresbased analysis, which is more suitable than routine analysis. Expression profile data were downloaded from the Gene Expression Omnibus database. A total of 503 genes were found to be differentially expressed, including 248 downregulated genes and 255 overexpressed genes. Network analysis identified 5 hub genes, including UBB, PIK3R1, MAPRE1, VEGFA, and ITGB1. Three of these, PIK3R1, VEGFA, and ITGB1, are known to be associated with preeclampsia or preeclampsia-6599 PLS analysis in preeclampsia ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 6598-6604 (2015) related biological processes. Our findings shed light on expression signatures of preeclampsia patients that can be used as theoretical support in future therapeutic studies.

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Identification of Differential Gene Expression Profiles in Placentas from Preeclamptic Pregnancies Versus Normal Pregnancies by DNA Microarrays

Cited by 69 publications

References 39 publications

Placental Macrophages Are Impaired in Chorioamnionitis, an Infectious Pathology of the Placenta

Placental Macrophages Are Impaired in Chorioamnionitis, an Infectious Pathology of the Placenta

Unsupervised Placental Gene Expression Profiling Identifies Clinically Relevant Subclasses of Human Preeclampsia

Partial least squares-based gene expression analysis in preeclampsia

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