Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of the first-trimester decidua for understanding the maintenance of early gestation as well as pathogenesis in pregnancy-related disorders

ABSTRACT: Implant failure and insufficient placental development are important causes of female infertility, recurrent miscarriage, and other pregnancy-related problems. A better understanding of gene expression profiling based on high-throughput sequencing technology is important for the study on the development of the placenta and the causes of pregnancy-related diseases. In this study, we collected 6 first-trimester chorionic villus and decidua tissues and obtained the transcriptome database on high-throughput sequencing. We performed routine principal component analysis (PCA) on these 12 samples and identified differentially expressed genes from samples with different sex background. And identified genes highly expressed in villus and decidua, respectively.

INSTRUMENT(S): Illumina Genome Analyzer II

ORGANISM(S): Homo sapiens

SUBMITTER: Liu Yajun

PROVIDER: E-MTAB-8181 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:AIMS/HYPOTHESIS: Pregnancies complicated by diabetes have a higher risk of adverse outcomes for mothers and children, including predisposition to disease later in life, such as metabolic syndrome and hypertension. We hypothesized that adverse outcomes from diabetic pregnancies may be linked to compromised placental function. Our goal in this study was to identify cellular and molecular abnormalities in diabetic placenta. METHODS: Using a mouse model of diabetic pregnancy, placental gene expression was assayed at midgestation and cellular composition was analyzed at various stages. Genome-wide expression profiling was validated by quantitative PCR, and tissue localization studies were performed to identify cellular correlates of altered gene expression in diabetic placenta. RESULTS: We detected significantly altered gene expression in diabetic placenta for genes expressed in the maternal as well as those in the embryonic compartments. We also found altered cellular composition of the decidual compartment. Furthermore, the junctional and labyrinth layers were reduced in diabetic placenta, accompanied by aberrant differentiation of spongiotrophoblast cells. CONCLUSIONS/INTERPRETATION: Diabetes during pregnancy alters transcriptional profiles in the murine placenta, affecting cells of both embryonic and maternal origin, and involving several genes not previously implicated in diabetic pregnancies. The molecular changes and abnormal differentiation of multiple cell types precede impaired growth of junctional zone and labyrinth, and placenta overall. Whether these changes represent direct responses to hyperglycaemia or physiological adaptations, they are likely to play a role in pregnancy complications and outcomes, and have implications for developmental origins of adult disease. The STZ diabetic mouse model was used to investigate gene expression changes in diabetic placentae at E10.5. Placentae were dissected from 5 different FVB dams at embryonic day 10.5 under diabetic conditions and from 5 control dams. Gene expression profiles from five individual placentae from independent pregnancies per group were compared.

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RNA-seq of the first-trimester decidua for understanding the maintenance of early gestation as well as pathogenesis in pregnancy-related disorders

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