Abstract
BackgroundIntrauterine growth restriction (IUGR) induces fetal cardiac remodelling and dysfunction, which persists postnatally and may explain the link between low birth weight and increased cardiovascular mortality in adulthood. However, the cellular and molecular bases for these changes are still not well understood. We tested the hypothesis that IUGR is associated with structural and functional gene expression changes in the fetal sarcomere cytoarchitecture, which remain present in adulthood.Methods and ResultsIUGR was induced in New Zealand pregnant rabbits by selective ligation of the utero-placental vessels. Fetal echocardiography demonstrated more globular hearts and signs of cardiac dysfunction in IUGR. Second harmonic generation microscopy (SHGM) showed shorter sarcomere length and shorter A-band and thick-thin filament interaction lengths, that were already present in utero and persisted at 70 postnatal days (adulthood). Sarcomeric M-band (GO: 0031430) functional term was over-represented in IUGR fetal hearts.ConclusionThe results suggest that IUGR induces cardiac dysfunction and permanent changes on the sarcomere.
Highlights
Intrauterine growth restriction (IUGR) is a major cause of perinatal mortality and long term morbidity [1] affecting up to 7– 10% of pregnancies
The results suggest that IUGR induces cardiac dysfunction and permanent changes on the sarcomere
While absolute fetal body and heart weights were significantly lower in IUGR, heart to body weight ratio was significantly increased in IUGR fetuses as compared to controls
Summary
Intrauterine growth restriction (IUGR) is a major cause of perinatal mortality and long term morbidity [1] affecting up to 7– 10% of pregnancies. IUGR results in low birth weight, which has been epidemiologically associated with an increased risk of cardiovascular disease in adulthood [2]. IUGR fetuses and newborns show signs of cardiovascular remodelling and dysfunction, including reduced annular peak velocities [7] and increased carotid intimamedia thickness [8]. These fetal changes persist postnatally, as shown in human children [9] and in adult animal models [10,11]. Intrauterine growth restriction (IUGR) induces fetal cardiac remodelling and dysfunction, which persists postnatally and may explain the link between low birth weight and increased cardiovascular mortality in adulthood. We tested the hypothesis that IUGR is associated with structural and functional gene expression changes in the fetal sarcomere cytoarchitecture, which remain present in adulthood
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