Abstract
Preeclampsia (PE) is a pregnancy-specific syndrome that causes substantial maternal and fetal morbidity and mortality. Increased production of antiangiogenic factors, soluble fms-like tyrosine kinase receptor-1 (sFlt-1) and soluble endoglin (sEng), as well as decreased circulating levels of free vascular endothelial growth factor (VEGF), contribute to the pathophysiology of PE. Our objective was to evaluate a novel placenta-related factor, tissue transglutaminase (tTG), in PE and to investigate the correlation among tTG and sFlt-1, sEng and VEGF levels in both normotensive pregnant patients and PE patients. A total of 205 pregnant primigravid women were recruited and divided into a normotensive group (n=100), a mild PE group (n=45) and a severe PE group (n=60). Circulating serum tTG, sFlt-1, sEng and free VEGF levels were determined using an enzyme-linked immunosorbent assay. The severe PE group showed higher levels of tTG, sFlt-1 and sEng than the mild PE and normotensive groups. Free VEGF levels were lower in the severe PE group than in the mild PE and normotensive groups. tTG correlated significantly with sFlt-1, sEng and VEGF in the PE groups, whereas this correlation was not observed in the normotensive group. The tTG, sFlt-1, sEng and VEGF levels showed a significant correlation with mean arterial pressure in the PE groups but not in the normotensive group. The tTG, sFlt-1, sEng and VEGF levels correlated with the degree of proteinuria. Our results reveal that tTG is associated with sFlt-1, sEng and VEGF in the maternal circulation of PE patients, suggesting that tTG may have a role in the pathogenesis of PE.
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We thank Guangzhou Medical College and Guangzhou Women and Children’s Medical Center for providing support and guidance.
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Cheng, M., He, P. & Fu, J. The relationship between circulating tissue transglutaminase, soluble fms-like tyrosine kinase-1, soluble endoglin and vascular endothelial growth factor in pre-eclampsia. J Hum Hypertens 30, 788–793 (2016). https://doi.org/10.1038/jhh.2016.32
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DOI: https://doi.org/10.1038/jhh.2016.32
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