The association between serum galectin-3 level and its placental production in patients with preeclampsia.

Abstract

Galectin-3 is β-galactoside-binding lectin, used in cardiology as a biomarker of heart failure. Available research suggest galectin-3 may play a role in the development of preeclampsia. Seventy seven women were included in the study: 39 with preeclampsia and 38 with uncomplicated pregnancy. Patients underwent blood sample analysis (galectin-3, N-terminal pro-brain natriuretic peptide (NT-proBNP), soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), cystatin C, creatinine) and echocardiographic examination. After delivery, placental tissue samples were obtained for immunohistochemistry evaluation. In patients with preeclampsia, serum galectin-3 levels (11.8 versus 9.5 ng/ml; p = 0.004) and galectin-3 expression in placental tissue (immunoreactive score (IRS) in extravillous trophoblasts: 9 versus 5; p = 0.002; in syncytiotrophoblasts: 6 versus 2, p < 0.001) were significantly higher than in the control group. Serum NT-proBNP and sFlt-1 levels, sFlt-1/PlGF ratio, serum creatinine and cystatin C levels were significantly higher, whereas serum PlGF levels and estimated glomerular filtration rate (eGFR) were significantly lower in preeclamptic patients than in uncomplicated pregnancy. On echocardiography, preeclamptic women had significantly greater thickness of interventricular septum (IVS) and left ventricle posterior wall (PW) and significantly worse left ventricle diastolic function (higher E/e' values). Serum galectin-3 level did not correlate with any other biochemical parameters, as well as the vast majority of echocardiographic parameters. Significant correlation between serum galectin-3 and its placental expression in syncytiotrophoblasts (STB) was revealed. Renal function parameters and NT-proBNP correlated with antiangiogenic state. This study demonstrated increased serum galectin-3 levels and placental galectin-3 production in preeclamptic patients, in comparison to women with uncomplicated pregnancy. Myocardial dysfunction and worse renal function parameters in patients with preeclampsia were not related to galectin-3. The main source of galectin-3 in maternal blood was its placental production. In the development of preeclampsia, galectin-3 may act as a compensatory mechanism to impaired placentation in early pregnancy.