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Spandidos Publications, Molecular Medicine Reports

DOI: 10.3892/mmr.2012.1141

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Increased expression levels of vitronectin in the maternal-fetal interface of placenta in early-onset severe preeclampsia

Journal article published in 2012 by Jing Shen, Xiaoyan, Xiaoyan Ma, Fei Yi, Azhar Rasul ORCID, Tonghui, Manhua Cui, Tonghui Ma ORCID
This paper is available in a repository.
This paper is available in a repository.

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Abstract

Preeclampsia (PE) is a pregnancy-specific disease, the pathogenesis of which remains unclear. The present study was designed to analyze whether vitronectin (VN), a multifunctional human glycoprotein, is expressed in PE and normal placentas. Furthermore, we aimed to explore VN expression profiles in relation to the pathogenesis of PE. Placental samples and plasma of early-onset severe PE (EOSP), late-onset severe PE (LOSP) and 2 control groups corresponding to EOSP and LOSP were collected. Immunohistochemistry, immunofluorescence and western blot analysis were used to detect VN protein expression profiles. mRNA expression levels of VN were detected by reverse transcription polymerase chain reaction (RT-PCR). The impact of VN on coagulation was investigated by comparing differences in coagulation parameters. Our results demonstrate that expression levels of VN in the maternal-fetal interface of the EOSP group are the highest (P<0.001). The expression levels of VN in descending order in infarct center, infarct edge, near infarct tissues and away from infarct tissues were identified (P<0.001). Immunofluorescence and immunoblotting were consistent with immunohistochemical results. The VN mRNA expression was detected. Prothrombin time (PT) was significantly shorter in EOSP compared with the control group (P<0.05), which had a significant negative correlation with expression levels of VN in the placental tissue of the group. VN may play a key role in repairing the lesions and limiting necrotic components into maternal blood through its adhesion. VN may be involved in the pathogenesis of EOSP by inducing an imbalance between coagulation and fibrinolysis.