Correlation between Soluble Endoglin, Vascular Endothelial Growth Factor Receptor-1, and Adipocytokines in Preeclampsia
Author(s) -
Hisashi Masuyama,
H Nakatsukasa,
Norio Takamoto,
Yuji Hiramatsu
Publication year - 2007
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jc.2006-2349
Subject(s) - medicine , preeclampsia , adipokine , adiponectin , endocrinology , placental growth factor , pathophysiology , vascular endothelial growth factor , endoglin , leptin , soluble fms like tyrosine kinase 1 , placenta , pregnancy , fetus , obesity , insulin resistance , biology , vegf receptors , genetics , stem cell , cd34
Context: Recent reports have demonstrated that soluble endoglin (sEng), an antiangiogenic protein thought to impair TGF-β binding to receptors, and soluble vascular endothelial growth factor receptor (sVEGFR)-1 play important roles in the pathophysiology of preeclampsia (PE). Moreover, insulin resistance, which is greatly influenced by adipocytokines, characterizes PE. Objectives: We examined possible links between sEng, VEGF, sVEGFR, and adipocytokines in the pathophysiology of PE. Study Design: We performed a cross-sectional study in 30 PE patients and controls matched for gestational age and body mass index. Blood samples were collected soon after disease onset. We measured serum concentrations of leptin, adiponectin, sEng, VEGF, placental growth factor (PlGF), and sVEGFR [soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble fetal liver kinase 1 (sFlk-1)], and examined the placental protein content of sEng and sFlt-1. Results: sEng concentrations in PE patients (60.9 ± 28.8 ng/ml) were significantly higher than those in controls (11.2 ± 4.4 ng/ml). There was a significant correlation between sEng and sFlt-1 or PlGF. Moreover, there were significant differences in mean blood pressure between the high and low sEng groups, and in proteinuria between the high and low sFlt-1 groups, and significant differences in placental sEng and sFlt-1 contents between patients with and without severe hypertension or proteinuria. sEng was also correlated positively with adiponectin levels and negatively with the leptin to adiponectin ratio. Conclusions: Along with sFlt-1 and PlGF, sEng might play a role in the pathophysiology of PE, especially in elevating blood pressure, while the association with hypoadiponectinemia and the high leptin to adiponectin ratio in pregnancy seem to be risk factors for PE.
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