Project description:Impaired muscle growth as a result of IUGR is a major contributor to lifelong reductions in muscle mass (sarcopenia) and metabolic disease risk. We use an ovine model of chronic placental insufficiency which restricts nutrient supply from mother to fetus and results in intrauterine growth restriction. In our model of placental insufficiency and IUGR, fetal hindlimb muscles weigh less than normally-grown control fetuses and have smaller myofiber diameters. Given the frequent correlation between functional changes and transcriptional changes, we investigated the effect of chronic placental insufficiency and IUGR on fetal skeletal muscle gene expression. We found that gene expression in the skeletal muscle is significantly altered by chronic placental insufficiency. In gene ontology analysis, we found that genes involved in cell cycle regulation were most significantly affected, with downregulation of several cyclins. These observations may in part account for decreased muscle weight relative to brain weight observed in the late gestation IUGR fetus.
Project description:Intrauterine growth restriction (IUGR) impairs fetal growth and development, perturbs nutrient metabolism, and increases the risk of developing diseases in the postnatal life. However, the underlying mechanisms by which IUGR affects fetuses remain incompletely understood. Here, we applied high-throughput proteomics approach and biochemical analysis to investigate the impact of IUGR on fetal liver.
Project description:The study objective was to determine differentially expressed mRNA transcripts in skeletal muscle from fetal sheep and 30 day old lambs to determine persistent gene changes following placental insufficiency-induced intrauterine growth restriction.
2023-08-17 | GSE123929 | GEO
Project description:Skeletal Muscle RNA-seq data of Intrauterine growth restriction (IUGR) and normal pig foetuses
Project description:Intrauterine growth restriction (IUGR) is associated with increased susceptibility to obesity, metabolic syndrome and type 2 diabetes. Although the mechanisms underlying the fetal origin of metabolic disease are poorly understood, evidence suggests epigenomic alterations play a critical role. We sought to identify changes in DNA methylation patterns that define IUGR in CD3+ T-cells purified from umbilical cord blood obtained from appropriate for gestational age (Control) and IUGR male newborns using a genome-wide assay. We identified a global shift towards hypermethylation in IUGR compared to Control newborns targeted to regulatory regions of the genome.
