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Objective: We analyzed changes in gene expression of placental growth factor (PIGF) in human placental samples obtained postpartum from pregnancies with IUGR.Methods: During a twelve-month study period representing the calendar year of 2012 placental samples from 101 pregnancies with IUGR and from 140 normal pregnancies were obtained for analysis of a potential difference in PIGF gene expression.Results: There was no significant difference in gene activity of the PIGF gene between the IUGR versus normal pregnancy groups (Ln2α: 0.92; p < 0.06). Within the IUGR group, no fetal gender-dependent differences were seen in placental PIGF gene expression (Ln2α: 0.72; p = 0.05). Placental PIGF gene activity was significantly lower in fetuses with more severe IUGR versus less severe cases (Ln2α: -1.49; p < 0.03).Conclusion: We found no difference in gene expression of PIGF in placental samples obtained from IUGR pregnancies versus normal pregnancy suggesting the absence of a direct role of PIGF gene activity in the development of defective angiogenesis in IUGR during the later stages of gestation. However, in more severe cases of intrauterine growth restriction PIGF expression does show a significant decrease indicating its potential role in the profound defect in angiogenesis in these cases. [ABSTRACT FROM AUTHOR]

Objective: The gene expression of transforming growth factor beta-1 (TGF-β1) 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-β1 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-β1 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-β1 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-β1 in placental samples obtained from SGA pregnancies versus normal pregnancy suggesting an absence of a direct role of the TGF-β1 gene in the development of SGA. However, the absence of increased gene expression of TGF-β1 in SGA can be conceptualized as a failure to mount a compensatory response in the SGA environment. [ABSTRACT FROM AUTHOR]

Objective: In this study, we assessed Bcl-2 and Bax gene expression patterns in human placental samples from intrauterine growth restriction (IUGR) pregnancies using normal pregnancy as control. Methods: We compared Bcl-2 and Bax gene expression in placental samples from all IUGR pregnancies treated in our clinic between 1 January 2010-1 January 2011 vs. 140 normal pregnancy samples from the same study period. We also assessed clinical parameters such as maternal age, gestational weight gain, gestational body mass index (BMI) change, and maternal birth weight. Results: In IUGR, the Bcl-2 gene was underexpressed compared to normal pregnancy. There was no difference in the Bax gene activity in the two groups. The degree of growth restriction within the IUGR group did not correlate with Bcl-2 or Bax gene activity. Conclusions: Our study revealed that it is the reduced inhibitory activity of the Bcl-2 gene rather than an enhanced stimulatory activity of the Bax gene in the background of the increased apoptosis observed in IUGR. IUGR appears to be more common with maternal age around 20 years and above 35 years. Gestational weight gain and gestational BMI change also predict the risk for IUGR. [ABSTRACT FROM AUTHOR]

Objective. The apoptotic genes Bax and Bcl-2 are both involved in the pathogenesis of preterm delivery in conjunction with additional factors. We characterized gene expression patterns of these apoptotic regulatory genes as well as relevant environmental factors. Design. A gene expression study with evaluation of clinical data. Setting. Semmelweis University, Budapest, Hungary. Sample. Human placental samples from 104 preterm and 140 full-term pregnancies. Methods. Gene tests were performed using real-time PCR to assess gene expression patterns of Bax and Bcl-2 in human placental samples. Clinical data were collected from our computerized database. Main outcome measures. Apoptotic gene expression pattern and clinical information against the background of preterm delivery. Results. In placental samples from preterm delivery pregnancies, expression of the Bcl-2 gene was unchanged, whereas the Bax gene was overexpressed. Placental gene expression of Bax in preterm delivery was dependent on gestational age with gestational weeks 28-32 and 32-36 associated with overexpression, and no overexpression in gestational weeks 24-28. Preterm delivery began with premature rupture of membranes in 70.2% and spontaneous uterine activity in 29.8%. Conclusions. The Bax gene was overexpressed in preterm delivery, whereas expression of the Bcl-2 gene remained unchanged. After the 28th gestational week, apoptosis appears to be a key factor in the pathogenesis of preterm delivery. [ABSTRACT FROM AUTHOR]

Introduction: In this study, we compared insulin-like growth factor (IGF)-gene expression patterns and characteristics of glucose and insulin metabolism in human placenta from pregnancies with or without intrauterine growth restriction (IUGR). Materials and methods: We compared 101 human placentas from intrauterine growth restriction pregnancies to those of 140 normal pregnancies treated at our department in a one-year period. We have also assessed the serum glucose and insulin levels of the IUGR and control groups. Several possible predicting factors of IUGR were also investigated. Results: Risk for IUGR was suggested by gestational weight gain and gestational increase in maternal body mass index (BMI) as well as maternal birthweight. In pregnancies without IUGR, umbilical cord glucose and insulin levels were significantly higher than in pregnancies with IUGR. In placentas from pregnancies with IUGR an overexpression of the IGF-2 and the insulin-like growth factor binding protein (IGFBP)-3 genes was found. In placentas from pregnancies with male fetal gender we found a significant overexpression of the IGF-2 gene. Discussion: Gestational weight gain and BMI increase seem to predict the development of IUGR. Insulin and carbohydrate metabolism are also impaired in IUGR fetuses. In the placentas from pregnancies with IUGR, IGF-2 is overexpressed reflecting its physiological role in optimizing energy distribution in a low-energy environment. [ABSTRACT FROM AUTHOR]