ABSTRACT
OBJECTIVE: The gene expression of transforming growth factor beta-1 (TGF-ß1) in human placental samples obtained from pregnancies with small for gestational age fetuses (SGA) was compared to those of normal pregnancies. METHODS: In 2011 placental samples from 101 pregnancies with SGA and from 140 normal pregnancies were obtained for analysis of TGF-ß1 gene expression. Several clinical parameters were also assessed for correlation between genetic and clinical parameters. RESULTS: There were no significant differences in gene activity of the TGF-ß1 gene between the SGA versus normal pregnancy groups (Ln2α: 0.16; p = 0.07). Within the SGA group, no fetal gender-dependent differences were seen in TGF-ß1 gene expression (Ln2α: −0.11; p = 0.05). Similarly, no significant differences in gene activity were observed by the degree of severity of SGA as assessed by percentile fetal birth-weight (Ln2α: 0.32; p = 0.06). CONCLUSION: We found no change in gene expression of TGF-ß1 in placental samples obtained from SGA pregnancies versus normal pregnancy suggesting an absence of a direct role of the TGF-ß1 gene in the development of SGA. However, the absence of increased gene expression of TGF-ß1 in SGA can be conceptualized as a failure to mount a compensatory response in the SGA environment.
Subject(s)
Fetal Growth Retardation/genetics , Gene Expression , Infant, Small for Gestational Age , Placenta/metabolism , Transforming Growth Factor beta1/genetics , Biomarkers/metabolism , Case-Control Studies , Female , Fetal Growth Retardation/metabolism , Humans , Infant, Newborn , Male , Pregnancy , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain Reaction , Transforming Growth Factor beta1/metabolismABSTRACT
Epigenetic factors are nowadays in the focus of scientific interest in medicine including obstetrics. The environment in utero and early neonatal life may induce a permanent response in the fetus and the newborn leading to enhanced susceptibility to later diseases. There is now growing evidence that the effects of developmental programming may also manifest themselves in the next generations without further suboptimal exposure. The so-called fetal programming may also highlight a tight connection between pathological conditions in pregnancy, environmental factors and the development of chronic diseases in adulthood. Investigation of epigenetic factors may yield new possibilities for the prevention of chronic diseases affecting a significant part of the population.
