Changes of placental syndecan-1 expression in preeclampsia and HELLP syndrome

Szilvia Szabo, Yi Xu, Roberto Romero, Tibor Fule, Katalin Karaszi, Gaurav Bhatti, Tibor Varkonyi, Ildiko Varkonyi, Tibor Krenacs, Zhong Dong, Adi L. Tarca, Tinnakorn Chaiworapongsa, Sonia S. Hassan, Zoltan Papp, Ilona Kovalszky, Nandor Gabor Than

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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.

Original languageEnglish
Pages (from-to)445-458
Number of pages14
JournalVirchows Archiv
Issue number3
Publication statusPublished - Sep 1 2013



  • Cell signaling
  • Pregnancy
  • Proteoglycan
  • Syncytiotrophoblast
  • Systemic inflammation
  • Virtual microscopy

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

Cite this

Szabo, S., Xu, Y., Romero, R., Fule, T., Karaszi, K., Bhatti, G., Varkonyi, T., Varkonyi, I., Krenacs, T., Dong, Z., Tarca, A. L., Chaiworapongsa, T., Hassan, S. S., Papp, Z., Kovalszky, I., & Than, N. G. (2013). Changes of placental syndecan-1 expression in preeclampsia and HELLP syndrome. Virchows Archiv, 463(3), 445-458.