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Submitted on October 12, 2004
Accepted on November 19, 2004
Department of Emergency and Organ Transplantation - Section on Internal Medicine, Endocrinology and Metabolic Diseases, University of Bari, Bari, Italy; Department of Obstetrics and Gynecology, Clinica Ostetrica e Ginecologica II, University of Bari, Bari, Italy; Obstetrics and Gynecology, University of Foggia, Foggia, Italy
* To whom correspondence should be addressed. E-mail: f.giorgino{at}endo.uniba.it.
The insulin-like growth factors (IGFs) promote growth and development of the feto-placental unit during gestation, and impairment in their placental actions may result in altered intra-uterine growth of the fetus. In this study, proteins involved in IGF signaling were investigated in human placentae from pregnancies complicated by intra-uterine growth restriction (IUGR) compared with those from normal pregnancies. IUGR placentae exhibited 33% reduction in the protein content of IGF-I receptors but no changes in insulin receptor protein levels. In addition, IRS-2 protein levels were reduced in IUGR placentae, with no changes in IRS-1 or Shc protein content, and this was associated with a parallel decrease in IRS-2-associated PI 3-kinase. Akt protein expression was also reduced in IUGR, whereas phosphorylation of Akt and of its substrate GSK-3 was unchanged. Finally, in IUGR placentae there was impaired activation of multiple members of the MAP kinase family, because phosphorylation of p38 and JNK was reduced 70%. In conclusion, human placentae from pregnancies complicated by IUGR are characterized by decreased IGF-I receptor content, selective impairment of the IRS-2/PI 3-kinase pathway, and reduced p38 and JNK activation. The observed abnormalities in IGF-I signaling may contribute to altered fetal growth and development in human IUGR.
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