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Real-time Analyses of Retinol Transport by the Membrane Receptor of Plasma Retinol Binding Protein
Published on: January 28, 2013
Retinol binding protein 4--a novel association with early-onset preeclampsia
Edi Vaisbuch1, Roberto Romero, Shali Mazaki-Tovi
1Intramural Division, Perinatology Research Branch, NICHD/NIH/DHHS, Hutzel Women's Hospital, Bethesda, MD, USA.
Insights
Maternal plasma RBP4 (Retinol Binding Protein 4) is elevated in preeclampsia (PE), particularly preterm PE. This adipokine may play a role in preterm PE pathogenesis, but not in small-for-gestational age neonates or fetal death.
Area of Science:
- Obstetrics and Gynecology
- Endocrinology
- Perinatal Medicine
Background:
- Adipokines, like Retinol Binding Protein 4 (RBP4), are implicated in pregnancy complications.
- Dysregulated adipokines may link metabolic issues and inflammation in conditions such as preeclampsia (PE), small-for-gestational age (SGA) neonates, and fetal death (FD).
- RBP4 is a novel adipokine involved in obesity and immune response regulation.
Purpose of the Study:
- To investigate maternal plasma RBP4 concentrations in normal pregnancy, PE, SGA neonates, and FD.
- To determine if RBP4 levels are associated with specific pregnancy complications.
Main Methods:
- Cross-sectional study design.
- Inclusion of 134 normal pregnancies, 104 PE cases, 28 SGA neonates, and 37 FD cases.
- Quantification of maternal plasma RBP4 using ELISA and analysis with non-parametric statistics.
Main Results:
- Maternal plasma RBP4 was significantly higher in PE patients compared to normal pregnancies (P=0.03).
- Preterm PE (<37 weeks) showed higher RBP4 levels than term PE (P=0.017) and normal pregnancies (P=0.002).
- No significant difference in RBP4 levels was observed between normal pregnancies and those with SGA neonates or FD.
Conclusions:
- Preeclampsia is associated with elevated maternal plasma RBP4, unlike SGA or FD.
- Higher RBP4 concentrations in preterm PE suggest a potential role in its pathogenesis.
- RBP4 does not appear to be involved in the pathogenesis of SGA or FD.
Objective:
Dysregulation of maternal circulating adipokines has been implicated in several "great obstetrical syndromes" including preeclampsia (PE), small-for-gestational age (SGA) neonate and fetal death (FD). It has been suggested that adipokines provide a molecular link between metabolic derangements and inflammatory response in complicated pregnancies. Retinol binding protein 4 (RBP4), a novel adipokine, plays a role in obesity-related disorders, as well as in the regulation of the immune response. The aim of this study was to determine whether there are changes in maternal plasma concentrations of RBP4 in patients with PE and in those with an SGA neonate or FD.
Study Design:
This cross-sectional study included patients in the following groups: 1) normal pregnancy (n=134); 2) PE (n=104); 3) SGA neonate (n=28); and 4) FD (n=37). Maternal plasma RBP4 concentrations were determined by ELISA. Non-parametric statistics were used for analysis.
Results:
1) The median maternal plasma RBP4 concentration was higher among patients with PE than in those with a normal pregnancy (P=0.03); 2) The median maternal plasma RBP4 concentrations of patients with preterm PE (<37 weeks) was higher than that of those with term PE (P=0.017) and than that of those with a normal pregnancy (P=0.002); 3) The median maternal plasma RBP4 concentration did not differ significantly between patients with a normal pregnancy and those with an SGA neonate or with an FD; 4) Among normal pregnant women, the maternal plasma RBP4 concentrations did not correlate with pre-pregnancy body mass index, gestational age at blood sampling and neonatal birthweight.
Conclusions:
1) Preeclampsia, but not pregnancy with an SGA neonate or an FD, is associated with a higher median maternal plasma concentration of RBP4 than normal pregnancy; 2) Preterm PE, and specifically early-onset PE, is associated with higher median RBP4 concentrations in maternal plasma compared to term PE. These findings suggest a role for RBP4 in the pathogenesis of preterm PE, but not in SGA and FD.
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