02909nas a2200373   4500008004100000022001400041245016200055210006900217260001300286300001300299490000800312520168000320653001202000653002702012653002202039653001102061653002902072653002002101653001702121653001502138653003002153653001302183653001402196653001202210100002802222700001802250700003302268700002002301700002902321700002002350700001802370700002202388856012502410       2013                        eng d  a1522-153900aIntrauterine growth restriction is associated with cardiac ultrastructural and gene expression changes related to the energetic metabolism in a rabbit model.0 aIntrauterine growth restriction is associated with cardiac ultra  c2013 Dec  aH1752-600 v3053 a<p>Intrauterine growth restriction (IUGR) affects 7-10% of pregnancies and is associated with cardiovascular remodeling and dysfunction, which persists into adulthood. The underlying subcellular remodeling and cardiovascular programming events are still poorly documented. Cardiac muscle is central in the fetal adaptive mechanism to IUGR given its high energetic demands. The energetic homeostasis depends on the correct interaction of several molecular pathways and the adequate arrangement of intracellular energetic units (ICEUs), where mitochondria interact with the contractile machinery and the main cardiac ATPases to enable a quick and efficient energy transfer. We studied subcellular cardiac adaptations to IUGR in an experimental rabbit model. We evaluated the ultrastructure of ICEUs with transmission electron microscopy and observed an altered spatial arrangement in IUGR, with significant increases in cytosolic space between mitochondria and myofilaments. A global decrease of mitochondrial density was also observed. In addition, we conducted a global gene expression profile by advanced bioinformatics tools to assess the expression of genes involved in the cardiomyocyte energetic metabolism and identified four gene modules with a coordinated over-representation in IUGR: oxygen homeostasis (GO: 0032364), mitochondrial respiratory chain complex I (GO:0005747), oxidative phosphorylation (GO: 0006119), and NADH dehydrogenase activity (GO:0003954). These findings might contribute to changes in energetic homeostasis in IUGR. The potential persistence and role of these changes in long-term cardiovascular programming deserves further investigation. </p>10aAnimals10aDisease Models, Animal10aEnergy Metabolism10aFemale10aFetal Growth Retardation10agene expression10aMitochondria10aMyocardium10aOxidative Phosphorylation10aPlacenta10aPregnancy10aRabbits1 aGonzález-Tendero, Anna1 aTorre, Iratxe1 aGarcía-Cañadilla, Patricia1 aCrispi, Fátima1 aGarcia-Garcia, Francisco1 aDopazo, Joaquin1 aBijnens, Bart1 aGratacós, Eduard  uhttp://clinbioinfosspa.es/content/intrauterine-growth-restriction-associated-cardiac-ultrastructural-and-gene-expression