Mus musculus
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ABSTRACT:
PROVIDER: PRJNA147589 | ENA |
REPOSITORIES: ENA
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Project description:Maternal diabetes causes cardiac malformations in fetuses. In this study, we have analyzed the differential gene expression profiling in the developing heart of embryos from diabetic and control mice by using the oligonucleotide microarray. Expression patterns of genes and proteins that are differentially expressed in the developing heart were further examined by the real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry. Embryos of diabetic pregnancies displayed cardiac malformations. Microarray analysis revealed the genes that were altered in expression level in the developing heart of embryos from diabetic mice when compared to controls. It is concluded that altered expression of a variety of genes involved in heart development is associated with cardiac malformations in offsprings of diabetic mother. We used microarrays to identify the genes specific to the developing heart of embryos from control and diabetic mice RNA was isolated from heart tissue of control and diabetes exposed E13.5 and E15.5 mouse embryos (three samples each). The RNA was hybridised onto Affymetrix Mouse Genome 430 2.0 Array.
2011-09-13 | E-GEOD-32078 | biostudies-arrayexpress
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.
2011-06-01 | E-GEOD-28277 | biostudies-arrayexpress
Project description:Maternal diabetes during early pregnancy can cause birth defects, notably of the developing heart and nervous system. To recognize the gene expression differences that may be the basis for such birth defects, we performed RNA-Seq on mouse embryos of the Non-Obese Diabetic (NOD) strain. Mice of that strain spontaneously develop type I diabetes.
2022-05-04 | GSE197396 | GEO
Project description:We generated the SRSF10 -/- mice, and collected their embryonic heart at 13.5 and controls. Then, we extracted RNAs of embryonic heart and performed next generation sequencing. By comparing sequcing data from WT and SRSF10 -/- samples, we profiled the alternative splicing events and gene expression regulated by SRSF10 during mouse heart development process. E13.5 embryonic heart mRNA profiles of wild type (WT) and SRSF10-/- mice were generated by deep sequencing, using Illumina HiSeq2000.
2015-04-01 | E-GEOD-66965 | biostudies-arrayexpress
Project description:Congenital heart defects (CHD) are one of the most common defects in offspring of diabetic mothers. There is a clear association between maternal diabetes and CHD; however the underlying molecular mechanism remains unknown. We hypothesized that maternal diabetes affects with the expression of early developmental genes that regulate the essential developmental processes of the heart, thereby resulting in the pathogenesis of CHD. We analyzed genome-wide expression profiling in the developing heart of embryos from diabetic and control mice by using the oligonucleotide microarray. Microarray analysis revealed that a total of 878 genes exhibited more than 1.5 fold changes in expression level in the hearts of experimental embryos in either E13.5 or E15.5 compared with their respective controls. Expression pattern of genes that is differentially expressed in the developing heart was further examined by the real-time reverse transcriptase-polymerase chain reaction. Several genes involved in a number of molecular signaling pathways such as apoptosis, proliferation, migration and differentiation in the developing heart were differentially expressed in embryos of diabetic pregnancy. It is concluded that altered expression of several genes involved in heart development may contribute to CHD in offspring of diabetic mothers.
2011-09-14 | GSE32078 | GEO
Project description:The understanding of protein alterations in the diabetic heart is of vital importance because of increased risk of cardiovascular co-morbidities. The study aims at elucidating metabolic pathways in the diabetic rat heart during development of Type 2 diabetes mellitus using MS based proteomics.
2018-06-26 | PXD009538 | Pride
Project description:The understanding of protein alterations in the diabetic heart is of vital importance because of increased risk of cardiovascular co-morbidities. The study aims at elucidating metabolic pathways in the diabetic rat heart during development of Type 2 diabetes mellitus using MS based proteomics.
2018-06-26 | PXD009554 | Pride
Project description:The understanding of protein alterations in the diabetic heart is of vital importance because of increased risk of cardiovascular co-morbidities. The study aims at elucidating metabolic pathways in the diabetic rat heart during development of Type 2 diabetes mellitus using MS based proteomics.
2018-06-26 | PXD009555 | Pride
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.
2011-06-01 | GSE28277 | GEO