Differentially expressed miRNAs in trisomy 21 placentas
Language English Country England, Great Britain Media print-electronic
Document type Journal Article
PubMed
27323694
DOI
10.1002/pd.4861
Knihovny.cz E-resources
- MeSH
- Adult MeSH
- Down Syndrome genetics metabolism MeSH
- Epidermal Growth Factor genetics MeSH
- Epigenesis, Genetic MeSH
- Gene Products, env genetics MeSH
- Inhibins genetics MeSH
- Cadherins genetics MeSH
- Connexin 43 genetics MeSH
- Real-Time Polymerase Chain Reaction MeSH
- Leptin genetics MeSH
- Humans MeSH
- MicroRNAs genetics metabolism MeSH
- Chorionic Villi Sampling MeSH
- Pilot Projects MeSH
- Placenta metabolism MeSH
- Placentation genetics MeSH
- Case-Control Studies MeSH
- Pregnancy Proteins genetics MeSH
- Pregnancy MeSH
- Transcriptome MeSH
- Up-Regulation MeSH
- Gene Expression Regulation, Developmental genetics MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Pregnancy MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Epidermal Growth Factor MeSH
- ERVFRD-1 protein, human MeSH Browser
- Gene Products, env MeSH
- GJA1 protein, human MeSH Browser
- inhibin-alpha subunit MeSH Browser
- Inhibins MeSH
- Cadherins MeSH
- Connexin 43 MeSH
- Leptin MeSH
- MicroRNAs MeSH
- MIRN10 microRNA, human MeSH Browser
- MIRN125 microRNA, human MeSH Browser
- MIRN542 microRNA, human MeSH Browser
- MIRN615 microRNA, human MeSH Browser
- MIRN99 microRNA, human MeSH Browser
- mirnlet7 microRNA, human MeSH Browser
- osteoblast cadherin MeSH Browser
- syncytin MeSH Browser
- Pregnancy Proteins MeSH
OBJECTIVE: Molecular pathogenesis of Down syndrome (DS) is still incompletely understood. Epigenetic mechanisms, including miRNAs gene expression regulation, belong to potential influencing factors. The aims of this study were to compare miRNAs expressions in placentas with normal and trisomic karyotype and to associate differentially expressed miRNAs with concrete biological pathways. METHODS: A total of 80 CVS samples - 41 with trisomy 21 and 39 with normal karyotype - were included in our study. Results obtained in the pilot study using real-time PCR technology and TaqMan Human miRNA Array Cards were subsequently validated on different samples using individual TaqMan miRNA Assays. RESULTS: Seven miRNAs were verified as upregulated in DS placentas (miR-99a, miR-542-5p, miR-10b, miR-125b, miR-615, let-7c and miR-654); three of these miRNAs are located on chromosome 21 (miR-99a, miR-125b and let-7c). Many essential biological processes, transcriptional regulation or apoptosis, were identified as being potentially influenced by altered miRNA levels. Moreover, miRNAs overexpressed in DS placenta apparently regulate genes involved in placenta development (GJA1, CDH11, EGF, ERVW-1, ERVFRD-1, LEP or INHA). CONCLUSION: These findings suggest the possible participation of miRNAs in Down syndrome impaired placentation and connected pregnancy pathologies. © 2016 John Wiley & Sons, Ltd.
References provided by Crossref.org
Genome-wide miRNA profiling in plasma of pregnant women with down syndrome fetuses
