title: [Fetal growth restriction and insulin-like growth factors].
abstract: The insulin-like growth factors (IGFs) and their receptors are implicated in pre- and postnatal growth and development. It is believed that the alteration in their activity may contribute to intrauterine growth restriction (IUGR). The aim of this experimental study was to relate some metabolic alterations, involving insulin-like growth factor pathway, in the placenta of pregnancies complicated by intrauterine growth restriction. Placental samples were obtained from six uncomplicated pregnancies and four pregnancies complicated by IUGR. These samples were then stained by immunohistochemical technique, using monoclonal antibodies. Our data have not shown a significant difference in the IR, the Shc isoforms and Akt levels between normal and IUGR placentas. The IUGR placentas had significantly lower levels of IRS-2 expression and higher levels of p85 transcription. IGF-I receptor binds to its ligand and activates two intracellular processes mainly a Shc-mediated pro-mitotic pathway and an anti-apoptotic pathway mediated by IRS and Akt. The diminished activity of one of the two pathways may alter the mitosis/apoptosis balance. Because of the low number of samples and the knowledge about the enzymatic pathways, we have not been able to associate our data to any biological consequence. We can only demonstrate that the enzymatic differences between IUGR and controls tend to the pro-apoptotic processes. It seems to be an other in vivo aspect in favour of the placental role in the IUGR pathogenesis.
authors: Dipartimento Scienze Chirurgiche Generali e Specialistiche, Sezione di Ginecologia ed Ostetricia, Università di Bari, Bari, Italia. marco.scioscia@tin.it
authors: M
authors: M
authors: Scioscia
authors: P
authors: P
authors: Greco
authors: A
authors: A
authors: Vimercati
authors: F
authors: F
authors: Giorgino
authors: S
authors: S
authors: Perrini
authors: L
authors: L
authors: Selvaggi
mesh_terms: D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D006801:Humans; D010920:Placenta / Q000737:chemistry*; D011247:Pregnancy; D013002:Somatomedins / Q000032:analysis*
chemical_list: D013002:Somatomedins