Changes of placental syndecan-1 expression in preeclampsia and HELLP syndrome
Autor: | Szilvia Szabo, Roberto Romero, Katalin Karaszi, Ilona Kovalszky, Tibor Várkonyi, Zoltán Papp, Tibor Füle, Adi L. Tarca, Yi Xu, Sonia S. Hassan, Tinnakorn Chaiworapongsa, Zhong Dong, Gaurav Bhatti, Tibor Krenács, Ildiko Varkonyi, Nandor Gabor Than |
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Rok vydání: | 2013 |
Předmět: |
Adult
HELLP Syndrome medicine.medical_specialty animal structures HELLP syndrome Placenta In Vitro Techniques Biology Article Pathology and Forensic Medicine Preeclampsia Syncytiotrophoblast Pre-Eclampsia Pregnancy Internal medicine medicine Humans Molecular Biology Cells Cultured Cytoskeleton reproductive and urinary physiology Cortical actin cytoskeleton Cell Differentiation Cell Biology General Medicine Apical membrane Bridged Bicyclo Compounds Heterocyclic medicine.disease Actin cytoskeleton Actins female genital diseases and pregnancy complications Hemolysis Trophoblasts carbohydrates (lipids) medicine.anatomical_structure Endocrinology Case-Control Studies embryonic structures Thiazolidines Female Syndecan-1 |
Zdroj: | Virchows Archiv. 463:445-458 |
ISSN: | 1432-2307 0945-6317 |
Popis: | Preeclampsia is characterized by maternal systemic anti-angiogenic and pro-inflammatory states. Syndecan-1 is a cell surface proteoglycan expressed by the syncytiotrophoblast, which plays an important role in angiogenesis and resolution of inflammation. Our aim was to examine placental syndecan-1 expression in preeclampsia with or without hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. Placentas were obtained from women in the following groups: (1) late-onset preeclampsia (n = 8); (2) early-onset preeclampsia without (n = 7) and (3) with HELLP syndrome (n = 8); (4) preterm controls (n = 5); and (5) term controls (n = 9). Tissue microarrays (TMAs) were constructed from paraffin-embedded placentas. TMA slides were immunostained for syndecan-1 and evaluated using microscopy, virtual microscopy, and semi-automated image analysis. Maternal sera from patients with preeclampsia (n = 49) and controls (n = 32) were immunoassayed for syndecan-1. BeWo cells were treated with Forskolin or Latrunculin B or kept in ischemic conditions. SDC1 expression and syndecan-1 production were investigated with qRT-PCR, confocal microscopy, and immunoassays. Syndecan-1 was localized to the syncytiotrophoblast apical membrane in normal placentas. Syndecan-1 immunoscores were higher in late-onset preeclampsia (p = 0.0001) and early-onset preeclampsia with or without HELLP syndrome (p = 0.02 for both) than in controls. Maternal serum syndecan-1 concentration was lower in preeclampsia (median, 673 ng/ml; interquartile range, 459-1,161 ng/ml) than in controls (1,158 ng/ml; 622-1,480 ng/ml). SDC1 expression and syndecan-1 immunostainings in BeWo cells and syndecan-1 concentrations in supernatants increased during cell differentiation. Disruption of the actin cytoskeleton with Latrunculin B decreased syndecan-1 release, while ischemic conditions increased it. Syncytiotrophoblastic syndecan-1 expression depends on the differentiation of villous trophoblasts, and trophoblastic syndecan-1 release is decreased in preeclampsia and HELLP syndrome. This phenomenon may be related to the disturbed syncytiotrophoblastic cortical actin cytoskeleton and associated with maternal anti-angiogenic and pro-inflammatory states in these syndromes. |
Databáze: | OpenAIRE |
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