Abstract
Alteration of placental development directly interferes with fetal growth. Epidermal growth factor (EGF) plays a major role in placental implantation, growth and differentiation. EGF acts on its placental target cells, ie the trophoblasts, via a specific receptor which belongs to the tyrosine kinase receptor family. Placental abundant EGF receptors(EGFR) localize in the brush border at the fetomaternal interface. EGFR expression is increased in vivo and in vitro with the differentiation of the syncytiotrophoblast which is the functional endocrine tissue of the placenta. In trophoblast cells in culture modulation of EGFR expression by hormones such as parathyroid-related peptide and retinoic acid or toxic substances such as smoke derived products interferes with placental endocrine functions. Interestingly, in microvilli purified from placenta of intrauterine growth retardation (IUGR) a decrease or absence of the EGFR tyrosine kinase activity is observed. This can be related to a decrease in EGFR expression in placenta with IUGR related to maternal toxemia. In some placentas with idiopathic IUGR a truncated form of EGFR lacking in tyrosine kinase activity, is observed. This suggests that an alteration of EGFR biological activity might interfere with the fetoplacental unit development.
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Evain-Brion, D., Alsat, E., Roulier, S. et al. PLACENTAL EPIDERMAL GROWTH FACTOR RECEPTORS: FROM PHYSIOLOGY TO PATHOLOGY. Pediatr Res 33 (Suppl 5), S7–S8 (1993). https://doi.org/10.1203/00006450-199305001-00031
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DOI: https://doi.org/10.1203/00006450-199305001-00031