Insulin-like growth factor-1 receptor expression in the placentae of diabetic and normal pregnancies

• Published in: Early human development 2007-01, Vol.83 (1), p.41-46
• Main Authors: Hayati, Abdul Rahman, Cheah, Fook Choe, Tan, Ay Eeng, Tan, Geok Chin
• Format: Article
• Language: English
• Subjects: Advanced Basic Science; Biological and medical sciences; Cardiomyopathy, Hypertrophic - etiology; Chorionic Villi - metabolism; Chorionic Villi - pathology; Decidua - metabolism; Decidua - pathology; Diabetes, Gestational - metabolism; Diabetes, Gestational - pathology; Embryology: invertebrates and vertebrates. Teratology; Endothelium - metabolism; Endothelium - pathology; Female; Fundamental and applied biological sciences. Psychology; Glucose Intolerance - metabolism; Glucose Intolerance - pathology; Humans; Immunohistochemistry; Infant, Newborn; Infant, Newborn, Diseases - etiology; Neonatal and Perinatal Medicine; Placenta - metabolism; Placenta - pathology; Pregnancy; Pregnancy in Diabetics - metabolism; Pregnancy in Diabetics - pathology; Receptor, IGF Type 1 - metabolism; Trophoblasts - metabolism; Trophoblasts - pathology
• ISSN: 0378-3782; 1872-6232
• DOI: 10.1016/j.earlhumdev.2006.04.002

Abstract Background Septal hypertrophic cardiomyopathy (sHCM) is a characteristic anomaly of the infant of diabetic mother (IDM). Insulin-like growth factor-1 (IGF-1) has been identified as a mediator of tissue overgrowth and we have previously shown that maternal IGF-1 levels were significantly elevated among neonates with asymmetrical sHCM. IGF-1 does not cross the placenta; it exerts physiologic action through binding to the IGF-1 receptor (IGF-1R). Localisation and expression of IGF-1R in term diabetic pregnancies are largely unclear. We have studied IGF-1R in the placentae of diabetic and normal pregnancies and this receptor expression in association with neonates with sHCM. Methods IGF-1R localization and expression in the placentae of six diabetic pregnancies associated with neonatal sHCM were compared with six each of randomly selected diabetic and normal pregnancies without neonatal sHCM by immunohistochemistry. The staining for IGF-1R in the deciduas, cytotrophoblasts, syncytiotrophoblasts and villous endothelium for these 18 samples were assessed and scored by two pathologists who were blinded to the respective diagnoses. Results Placental IGF-1R staining was negative in the villous endothelium for all three groups. IGF-1R staining was present in deciduas, cytotrophoblasts and syncytiotrophoblasts but the staining was weaker in the entire group of infants with sHCM compared to those without sHCM. Conclusions IGF-1R is localized in all cell types of the placenta except in villous endothelium. Weaker placental IGF-1R staining in the placentae of diabetic pregnancies associated with sHCM suggests reduced expression of IGF-1R. This may be a down-regulatory response to elevated maternal IGF with neonatal sHCM outcome.