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首页> 外文OA文献 >Intrauterine Wachstumsretardierung (IUGR) mit ARED-Flow in der Dopplersonographie der Arteria umbilicalis : molekulargenetische Analyse der Gene IGF-I und IGF-IR
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Intrauterine Wachstumsretardierung (IUGR) mit ARED-Flow in der Dopplersonographie der Arteria umbilicalis : molekulargenetische Analyse der Gene IGF-I und IGF-IR

机译：脐动脉多普勒超声检查中具有ARED流动的宫内发育迟缓（IUGR）：IGF-I和IGF-IR基因的分子遗传分析

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摘要

The objective of the present study was to evaluate a possible role of mutations of the genes IGF-I (Insulin-like Growth Factor-I) and IGF-IR (Insulin-like Growth Factor-I Receptor) in the pathogenesis of intrauterine growth retardation/ restriction (IUGR) with ARED (Absent or Reversed EndDiastolic)-flow in the Doppler ultrasonography of the A.umbilicalis. IUGR is caused by abnormal development of the placenta. The proliferation and differentiation of the villous trophoblast are predominantly controlled by growth factor IGF-I and its receptor IGF-IR. The functional IGF-I-system is also involved in the placental angiogenesis. Reduced activity of this system seems to be associated with an impaired proliferation of cytotrophoblastic cells and an inadequate placental angiogenesis, resulting in a postplacental hypoxia. The morphological changes of the placenta, as described above, are characteristic for pregnancies with IUGR and ARED-flow. In pregnancies with IUGR and PED (Preserved EndDiastolic)-flow in the presence of a bilateral abnormal uterine artery Doppler waveform (Notch), the placental histology shows a netlike arrangement of capillaries, forming multiply branched terminal villi (uteroplacental hypoxia). In the present study have been analyzed the genes encoding for IGF-I and IGF-IR in an IUGR/ARED-flow-group (19 mothers and their 19 fetuses) and an IUGR/PED-flow-group (14 mothers and their 14 fetuses). DNA was extracted from blood samples (mothers and alive fetuses) and paraffinblock samples (not-alive fetuses). Both genes were screened for genomic variants by single-strand conformation analysis (SSCP), restriction assays (RFLP) and direct sequencing. In the IGF-I-gene no variants could be identified in the study population. As for the IGF-IR-gene, five variants could be identified, three of them so far unknown: one in the 5´- and two in the 3´-untranslated region of the gene, as well as two polymorphisms that had already been described before in the literature: a silent mutation in exon 16 and a deletion in the 3´-untranslated region of the gene. The new polymorphisms were localized in the non-coding region of the IGF-IR-gene. Furthermore, all genomic variants were detected in similar frequencies in the patient-group and the control-group. Thus we conclude that the identified gene-polymorphisms do not play a relevant role in the aetiology of IUGR with ARED-flow.
机译：本研究的目的是评估IGF-I（胰岛素样生长因子-I）和IGF-IR（胰岛素样生长因子-I受体）基因突变在宫内发育迟缓的发病机制中的可能作用。脐动脉多普勒超声检查中的ARED（无或舒张末期舒张期）流/限制（IUGR）。 IUGR是由胎盘异常发育引起的。绒毛滋养层细胞的增殖和分化主要受生长因子IGF-1及其受体IGF-1R的控制。功能性IGF-I系统也参与胎盘血管生成。该系统活性降低似乎与细胞滋养层细胞的增殖受损和胎盘血管生成不足有关，导致胎盘后缺氧。如上所述，胎盘的形态变化是妊娠IUGR和ARED流的特征。在存在双侧子宫异常多普勒波形（Notch）的IUGR和PED（保留舒张末期）流动的妊娠中，胎盘组织学显示毛细血管呈网状排列，形成多分支末端绒毛（子宫胎盘低氧）。在本研究中，已经分析了IUGR / ARED流动组（19名母亲和19名胎儿）和IUGR / PED流动组（14名母亲和14名胎儿）中IGF-1和IGF-1R的编码基因。胎儿）。从血液样本（母亲和活着的胎儿）和石蜡块样本（未存活的胎儿）中提取DNA。通过单链构象分析（SSCP），限制性酶切测定（RFLP）和直接测序，筛选了两个基因的基因组变异。在IGF-I基因中，无法在研究人群中鉴定出变体。至于IGF-IR基因，可以鉴定出五个变体，其中三个迄今未知：一个位于该基因的5′-非翻译区域中，两个位于3′-非翻译区域中，以及两个已经被鉴定出的多态性。之前在文献中描述过：基因第16外显子的沉默突变和基因3'非翻译区的缺失。新的多态性位于IGF-IR基因的非编码区域。此外，在患者组和对照组中以相似的频率检测到所有基因组变体。因此，我们得出的结论是，已鉴定的基因多态性在具有ARED流的IUGR的病因中不发挥相关作用。

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    Kapagerof Athina;

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  • 年度 2006
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