Abstract
IntroductionThe human placenta expresses the IGF-I and IGF-IR proteins and their intracellular signal components (IRS-1, AKT and mTOR). The aim of this study was to assess the IGF-IR content and activation of downstream signaling molecules in placentas from newborns who were classified by gestational age and birth weight. We studied placentas from 25 term appropriate (T-AGA), 26 term small (T-SGA), 22 preterm AGA (PT-AGA), and 20 preterm SGA (PT-SGA) newborns. The total and phosphorylated IGF-IR, IRS-1, AKT, and mTOR contents were determined by Western Blot and normalized by actin or with their respective total content. The effect of IGF-I was determined by stimulating placental explants with recombinant IGF-I 10-8 mol/L for 15, 30, and 60 minutes.ResultsThe IGF-IR content was higher in T-SGA compared to T-AGA placentas, and the IRS-1 content was higher in PT-placentas compared with their respective T-placentas. The effect of IGF-I on the phosphorylated forms of IGF-IR was increased in T-SGA (150%) and PT-SGA (300%) compared with their respective AGA placentas. In addition, AKT serine phosphorylation was higher in PT-SGA compared to PT-AGA and T-SGA placentas (90% and 390% respectively).ConclusionThe higher protein content and response to IGF-I of IGF-IR, IRS-1, and AKT observed in SGA placentas may represent a compensatory mechanism in response to fetal growth restriction.
Highlights
The human placenta expresses the insulin-like growth factors (IGFs)-I and IGF-IR proteins and their intracellular signal components (IRS-1, AKT and mTOR)
The IGF-IR content was higher in T-small for gestational age (SGA) compared to T-appropriate for gestational age (AGA) placentas, and the insulin receptor substrate (IRS)-1 content was higher in PTplacentas compared with their respective T-placentas
The effect of IGF-I on the phosphorylated forms of IGF-IR was increased in T-SGA (150%) and preterm SGA (PT-SGA) (300%) compared with their respective AGA placentas
Summary
The human placenta expresses the IGF-I and IGF-IR proteins and their intracellular signal components (IRS-1, AKT and mTOR). Intrauterine growth restriction (IUGR) is an important obstetrical problem and refers to a fetus that has not reached its growth potential [1]. This condition may be the consequence of maternal, fetal, or placental factors. Recent advances in neonatal care have led to an improvement in the clinical outcome of premature infants (gestational age ,37 weeks). Some of these infants develop both [6] early and late morbidities, which may include motor, cognitive, visual, hearing, social-emotional, growth and metabolic problems [7]
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