Expression of glycodelin A in decidual tissue of preeclamptic, HELLP and intrauterine growth-restricted pregnancies
Expression of glycodelin A in decidual tissue of preeclamptic, HELLP and intrauterine growth-restricted pregnancies
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DOI：
10.1007/s00428-004-1201-3
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发表时间：
2005-04-01
期刊：
影响因子：
3.5
通讯作者：
Friese, K
中科院分区：
文献类型：
--
作者：
Jeschke, U;Kunert-Keil, C;Friese, K
在怀孕期间，胎盘产生各种蛋白质，这些蛋白质负责建立对母胎的耐受和循环。本研究旨在探讨糖蛋白A(PP14)在胎儿宫内生长受限(IUGR)胎盘蜕膜组织、子痫前期患者、溶血、肝功能亢进、低血小板(HELLP)患者及正常蜕膜组织中的表达。将IUGR患者、子痫前期患者、HELLP患者和正常足月胎盘组织石蜡包埋的蜕膜组织切片分别与抗糖蛋白A多克隆抗体或单抗孵育，ABC试剂染色。用半定量评分分析玻片上的免疫组织化学反应强度。用原位杂交法分析糖蛋白mRNA的表达。用单抗、多克隆抗体和原位杂交方法研究了IUGR和HELLP胎盘蜕膜细胞糖蛋白A的表达。然而，子痫前期蜕膜组织中糖蛋白mRNA的表达强度与正常胎盘组织相比无显著差异。蜕膜细胞糖蛋白A的表达减少似乎与IUGR和HELLP有关。因此，糖蛋白A可能在这些疾病的发病机制中起重要作用。
During pregnancy, the placenta produces a variety of proteins that are responsible for the establishment of the foeto-maternal tolerance and circulation. The aim of this study was to investigate the expression of glycodelin A (formerly named PP14) in decidual tissue of placentas with intrauterine growth restriction (IUGR), preeclamptic patients, hemolysis, elevated liver, low-platelet (HELLP) patients and normal decidual tissue. Slides of paraffin-embedded decidual tissue of patients with IUGR, preeclamptic patients, HELLP patients and normal-term placentas were incubated with either polyclonal or monoclonal antibodies against glycodelin A. Staining reaction was performed with the ABC reagent. Intensity of immunohistochemical reaction on the slides was analysed using a semi-quantitative score. In addition, expression of glycodelin mRNA was analysed by in situ hybridisation. Expression of glycodelin A was significantly reduced in decidual cells of placentas with IUGR and HELLP, as investigated with both monoclonal and polyclonal antibodies and in situ hybridisation. However, preeclamptic decidual tissue showed no significantly different expression of intensity of glycodelin mRNA compared with normal placental tissue controls. A reduced expression of glycodelin A by decidual cells seems to be related to IUGR and HELLP. Therefore, glycodelin A might play an important role in the pathogeneses of these diseases.