Landscape of Transcriptional Deregulations in the Preeclamptic Placenta

Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a default in the process of implantation, the placenta of preeclamptic women undergoes insufficient vascularization. This results in placental is...

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Veröffentlicht in:PloS one Jg. 8; H. 6; S. e65498
Hauptverfasser: Vaiman, Daniel, Calicchio, Rosamaria, Miralles, Francisco
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Public Library of Science 13.06.2013
Public Library of Science (PLoS)
Schlagworte:
Anopheles
Apoptosis
Binding Sites
Biology
Blood pressure
Cluster Analysis
Comparative analysis
Cyclic AMP response element-binding protein
Datasets
Deoxyribonucleic acid
Deregulation
DNA
DNA binding proteins
DNA damage
DNA microarrays
Female
Fetuses
Gene expression
Gene Expression Profiling
Gene Expression Regulation
Genes
Genetic aspects
Health aspects
Humans
Hypoxia
Implantation
Inflammation
Ischemia
Kinases
Maternal mortality
Medicine
Molecular modelling
Molecular Sequence Annotation
Morbidity
Mortality
NF-κB protein
Placenta
Placenta - metabolism
Pre-eclampsia
Pre-Eclampsia - genetics
Pre-Eclampsia - metabolism
Preeclampsia
Pregnancy
Pregnant women
Promoter Regions, Genetic
Promoters
Protein Binding
Protein Interaction Maps
Sp1 protein
Studies
Transcription (Genetics)
Transcription factors
Transcription Factors - genetics
Transcription Factors - metabolism
Transcription, Genetic
Vascularization
Vasoactive agents
ISSN:1932-6203, 1932-6203
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Abstract Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a default in the process of implantation, the placenta of preeclamptic women undergoes insufficient vascularization. This results in placental ischemia, inflammation and subsequent release of placental debris and vasoactive factors in the maternal circulation causing a systemic endothelial activation. Several microarray studies have analyzed the transcriptome of the preeclamptic placentas to identify genes which could be involved in placental dysfunction. In this study, we compared the data from publicly available microarray analyses to obtain a consensus list of modified genes. This allowed to identify consistently modified genes in the preeclamptic placenta. Of these, 67 were up-regulated and 31 down-regulated. Assuming that changes in the transcription level of co-expressed genes may result from the coordinated action of a limited number of transcription factors, we looked for over-represented putative transcription factor binding sites in the promoters of these genes. Indeed, we found that the promoters of up-regulated genes are enriched in putative binding sites for NFkB, CREB, ANRT, REEB1, SP1, and AP-2. In the promoters of down-regulated genes, the most prevalent putative binding sites are those of MZF-1, NFYA, E2F1 and MEF2A. These transcriptions factors are known to regulate specific biological pathways such as cell responses to inflammation, hypoxia, DNA damage and proliferation. We discuss here the molecular mechanisms of action of these transcription factors and how they can be related to the placental dysfunction in the context of preeclampsia.
AbstractList Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a default in the process of implantation, the placenta of preeclamptic women undergoes insufficient vascularization. This results in placental ischemia, inflammation and subsequent release of placental debris and vasoactive factors in the maternal circulation causing a systemic endothelial activation. Several microarray studies have analyzed the transcriptome of the preeclamptic placentas to identify genes which could be involved in placental dysfunction. In this study, we compared the data from publicly available microarray analyses to obtain a consensus list of modified genes. This allowed to identify consistently modified genes in the preeclamptic placenta. Of these, 67 were up-regulated and 31 down-regulated. Assuming that changes in the transcription level of co-expressed genes may result from the coordinated action of a limited number of transcription factors, we looked for over-represented putative transcription factor binding sites in the promoters of these genes. Indeed, we found that the promoters of up-regulated genes are enriched in putative binding sites for NFkB, CREB, ANRT, REEB1, SP1, and AP-2. In the promoters of down-regulated genes, the most prevalent putative binding sites are those of MZF-1, NFYA, E2F1 and MEF2A. These transcriptions factors are known to regulate specific biological pathways such as cell responses to inflammation, hypoxia, DNA damage and proliferation. We discuss here the molecular mechanisms of action of these transcription factors and how they can be related to the placental dysfunction in the context of preeclampsia.
Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a default in the process of implantation, the placenta of preeclamptic women undergoes insufficient vascularization. This results in placental ischemia, inflammation and subsequent release of placental debris and vasoactive factors in the maternal circulation causing a systemic endothelial activation. Several microarray studies have analyzed the transcriptome of the preeclamptic placentas to identify genes which could be involved in placental dysfunction. In this study, we compared the data from publicly available microarray analyses to obtain a consensus list of modified genes. This allowed to identify consistently modified genes in the preeclamptic placenta. Of these, 67 were up-regulated and 31 down-regulated. Assuming that changes in the transcription level of co-expressed genes may result from the coordinated action of a limited number of transcription factors, we looked for over-represented putative transcription factor binding sites in the promoters of these genes. Indeed, we found that the promoters of up-regulated genes are enriched in putative binding sites for NFkB, CREB, ANRT, REEB1, SP1, and AP-2. In the promoters of down-regulated genes, the most prevalent putative binding sites are those of MZF-1, NFYA, E2F1 and MEF2A. These transcriptions factors are known to regulate specific biological pathways such as cell responses to inflammation, hypoxia, DNA damage and proliferation. We discuss here the molecular mechanisms of action of these transcription factors and how they can be related to the placental dysfunction in the context of preeclampsia.Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a default in the process of implantation, the placenta of preeclamptic women undergoes insufficient vascularization. This results in placental ischemia, inflammation and subsequent release of placental debris and vasoactive factors in the maternal circulation causing a systemic endothelial activation. Several microarray studies have analyzed the transcriptome of the preeclamptic placentas to identify genes which could be involved in placental dysfunction. In this study, we compared the data from publicly available microarray analyses to obtain a consensus list of modified genes. This allowed to identify consistently modified genes in the preeclamptic placenta. Of these, 67 were up-regulated and 31 down-regulated. Assuming that changes in the transcription level of co-expressed genes may result from the coordinated action of a limited number of transcription factors, we looked for over-represented putative transcription factor binding sites in the promoters of these genes. Indeed, we found that the promoters of up-regulated genes are enriched in putative binding sites for NFkB, CREB, ANRT, REEB1, SP1, and AP-2. In the promoters of down-regulated genes, the most prevalent putative binding sites are those of MZF-1, NFYA, E2F1 and MEF2A. These transcriptions factors are known to regulate specific biological pathways such as cell responses to inflammation, hypoxia, DNA damage and proliferation. We discuss here the molecular mechanisms of action of these transcription factors and how they can be related to the placental dysfunction in the context of preeclampsia.
Audience Academic
Author Miralles, Francisco
Vaiman, Daniel
Calicchio, Rosamaria
AuthorAffiliation Otto-von-Guericke University Magdeburg, Germany
INSERM U1016-CNRS UMR8104, Université Paris Descartes, Institut Cochin, Paris, France
AuthorAffiliation_xml – name: INSERM U1016-CNRS UMR8104, Université Paris Descartes, Institut Cochin, Paris, France
– name: Otto-von-Guericke University Magdeburg, Germany
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  givenname: Rosamaria
  surname: Calicchio
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– sequence: 3
  givenname: Francisco
  surname: Miralles
  fullname: Miralles, Francisco
BackLink https://www.ncbi.nlm.nih.gov/pubmed/23785430$$D View this record in MEDLINE/PubMed
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Conceived and designed the experiments: DV FM. Performed the experiments: DV RC FM. Analyzed the data: DV RC FM. Wrote the paper: DV FM.
Competing Interests: The authors have declared that no competing interests exist.
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Snippet Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a...
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StartPage e65498
SubjectTerms Anopheles
Apoptosis
Binding Sites
Biology
Blood pressure
Cluster Analysis
Comparative analysis
Cyclic AMP response element-binding protein
Datasets
Deoxyribonucleic acid
Deregulation
DNA
DNA binding proteins
DNA damage
DNA microarrays
Female
Fetuses
Gene expression
Gene Expression Profiling
Gene Expression Regulation
Genes
Genetic aspects
Health aspects
Humans
Hypoxia
Implantation
Inflammation
Ischemia
Kinases
Maternal mortality
Medicine
Molecular modelling
Molecular Sequence Annotation
Morbidity
Mortality
NF-κB protein
Placenta
Placenta - metabolism
Pre-eclampsia
Pre-Eclampsia - genetics
Pre-Eclampsia - metabolism
Preeclampsia
Pregnancy
Pregnant women
Promoter Regions, Genetic
Promoters
Protein Binding
Protein Interaction Maps
Sp1 protein
Studies
Transcription (Genetics)
Transcription factors
Transcription Factors - genetics
Transcription Factors - metabolism
Transcription, Genetic
Vascularization
Vasoactive agents
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Title Landscape of Transcriptional Deregulations in the Preeclamptic Placenta
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