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首页> 外文期刊>Early human development >Insulin-like growth factor-1 receptor expression in the placentae of diabetic and normal pregnancies.
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Insulin-like growth factor-1 receptor expression in the placentae of diabetic and normal pregnancies.

机译:糖尿病和正常妊娠胎盘中胰岛素样生长因子-1受体的表达。

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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.
机译:背景:中隔肥厚型心肌病(sHCM)是糖尿病母亲(IDM)婴儿的特征性异常。胰岛素样生长因子-1(IGF-1)已被确定为组织过度生长的介体,并且我们先前已经证明,不对称sHCM的新生儿中孕妇的IGF-1水平显着升高。 IGF-1不能穿过胎盘。它通过与IGF-1受体(IGF-1R)结合而发挥生理作用。在足月糖尿病妊娠中IGF-1R的定位和表达尚不清楚。我们已经研究了糖尿病和正常妊娠胎盘中的IGF-1R,并且该受体的表达与sHCM新生儿有关。方法:采用免疫组织化学技术,比较了6例与新生儿sHCM相关的糖尿病孕妇和随机选择的6例无新生儿sHCM的糖尿病及正常孕妇在胎盘中IGF-1R的定位和表达。两名病理学家对这18个样品的蜕皮,细胞滋养细胞,合胞体滋养细胞和绒毛状内皮中的IGF-1R染色进行了评估并评分,他们对各自的诊断不知情。结果:所有三组的绒毛内皮细胞胎盘IGF-1R染色均为阴性。蜕皮,成纤维细胞和合体滋养细胞中存在IGF-1R染色,但与没有sHCM的婴儿相比,整个sHCM婴儿的染色均较弱。结论:IGF-1R定位于所有细胞类型的胎盘,除了绒毛状内皮。与sHCM相关的糖尿病孕妇胎盘中胎盘的IGF-1R染色较弱,提示IGF-1R的表达降低。这可能是对母亲IGF升高与新生儿sHCM结果的下调反应。

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