Project description:Epidemiologic studies have clearly identified modifications of fetal environment as a risk factor for the development of cardiovascular diseases and of metabolic syndrome in adulthood. In our experimental model, rats exposed to maternal diabetes develop a volume-dependent hypertension as early as 6 month of age. In order to determine if the development of hypertension results from an abnormal vascular fetal programming, gene expression profile of thoracic aorta were studied in adult rats exposed in utero to maternal hyperglycemia.
Project description:Maternal diabetes is associated with a wide range of fetal and neonatal adverse effects including pulmonary disturbances. To investigate the effects of maternal diabetes on neonatal lung gene expression profile, we performed microarray analysis on the lungs of 14-day-old rats born to diabetic dam. Keywords: disease state analysis Four neonatal lungs exposed to maternal diabetes and four control lungs were analyzed.
Project description:Context: Context: Gestational diabetes (GDM) has profound effects on the intrauterine metabolic milieu and is linked to obesity and diabetes in offspring, but the mechanisms driving these effects remain largely unknown. Alterations gene expression in amniocytes exposed to GDM in utero may identify potential mechanisms leading to metabolic dysfunction later in life. Objective: Objective: To profile changes in the transcriptome in human amniocytes exposed to GDM Methods: A nested case-control study was performed in second trimeseter amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis, gestational age at birth and gestational diabetes status. Sex-specific RNA-sequencing was completed and gene expression changes were identified. Results: Expression of interferon-stimulated genes was increased in GDM amniocytes accounting for 6 of the top 10 altered genes (q<0.05). Enriched biological pathways in GDM anmiocytes included pathways involving inflammation, the interferon response, fatty liver disease, monogenic diabetes and atherosclerosis. Conclusion: In a unique repository of human amniocytes exposed to GDM in utero, trancriptome analysis identified enrichment of inflammation and interferon-related pathways.
Project description:To explore the gene expression prolife in the chroniclly hypoxic myocardium, 8 rats were divided randomly into normoxic (n=4) or chroniclly hypoxic (n=4) group, and were exposed to room air (21% O2) or continued hypoxia (10% O2) for 4 weeks. Heart tissues were collected and RNA sequencing was applied to detect the overall gene expression prolife. Genes with adjusted P-value ≤0.01 (corrected by Benjamini-Hochberg) and |log2_ratio|≥0.585 are identified as differentially expressed genes. RNA sequencing identified a total of 2014 gene with statistical significances, among which 1260 genes were significantlly increased and 754 genes were significantlly decreased. The results showed that gene expression profiling was perturbed in chronically hypoxic myocardium.
Project description:Long non-coding RNA expression profile in the kidney of male low birth weight rats exposed to maternal protein restriction at postnatal day 10
Project description:We analysed the combined effects of exposure to maternal diabetes and disrupted HIF-1 signaling on the transcriptom in cardiac left ventricles of 12 weeks old male mice. This approach provides the information about the long term changes originating in utero due to maternal diabetes and inefficient response to hypoxia which develops as a result of hyperglycemia. The majority of changes were detected in Hif1a insufficient mice exposed to maternal diabetes.