Abstract 35
Background: IGF-I and its receptor (IGF-IR) have been implicated in the regulation of fetal growth, however, little is known about the pharmacology and in situ localization of functional IGF-I binding sites in the placenta. Methods: We describe IGF-I binding characteristics in human placenta at 14, 24 and 40 weeks gestation and in situ localization of IGF-I binding sites by autoradiography and immunocytochemistry. Results: Binding of [125I]IGF-I to placental cryosections was specific and halfmaximally inhibited by 7.9 ± 0.4, 1.1 ± 0.2 and 0.9 ± 0.2 × 10-9 M IGF-I at 14, 24 and 40 weeks gestation, respectively, demonstrating an increase in affinity of binding sites between 14 and 24 weeks and similar affinity later. Des(1-3) IGF-I inhibited binding of [125I]IGF-I at 4.5 ± 0.7, 0.5 ± 0.1 and 0.2 ± 0.1 × 10-9 M IGF-I indicating that this binding occurred to a smaller portion of specific IGF-IR and IGFBP-3 and a larger portion of different IGF-I binding species. Autoradiography localized [125I]IGF-I binding to decidua and trophoblast cells, in the latter with a shift from the cytotrohoblast (week 14) to the syncytiotrophoblast (week 40). Towards term enhanced [125I]IGF-I binding occurred to fetal vessels, the highest binding density was localized to trophoblast of the stem/intermediate villi. Immunocytochemistry showed an identical pattern of IGF-IR localization. Conclusions: Our results indicate that [125I]IGF-I binds to cells that are responsible for placental growth in early pregnancy and for fetal growth during later gestation. The high binding to trophoblast underlines the importance of the IGF-system in placental development.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Birnbacher, R., Pollak, A., Amann, G. et al. Pharmacological characterization and cellular localization oF IGF-I binding to placenta during pregnancy. Pediatr Res 45, 893 (1999). https://doi.org/10.1203/00006450-199906000-00053
Issue Date:
DOI: https://doi.org/10.1203/00006450-199906000-00053