Correlation between soluble endoglin, vascular endothelial growth factor receptor-1, and adipocytokines in preeclampsia.
BACKGROUND
Recent reports have demonstrated that soluble endoglin (sEng), an antiangiogenic protein thought to impair TGF-beta 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.


OBJECTIVE
We examined possible links between sEng, VEGF, sVEGFR, and adipocytokines in the pathophysiology of PE.


METHODS
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.
Masuyama
Hisashi
H
Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Shikata, Okayama 700-8558, Japan. masuyama@cc.okayama-u.ac.jp
Nakatsukasa
Hideki
H
Takamoto
Norio
N
Hiramatsu
Yuji
Y
D052242:Adiponectin / Q000097:blood*; D000328:Adult; D015703:Antigens, CD / Q000097:blood*; D001794:Blood Pressure; D000071063:Endoglin; D005260:Female; D006801:Humans; D020738:Leptin / Q000097:blood*; D010920:Placenta / Q000378:metabolism; D000072483:Placenta Growth Factor; D011225:Pre-Eclampsia / Q000453:epidemiology / Q000378:metabolism*; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000097:blood; D011956:Receptors, Cell Surface / Q000097:blood*; D012307:Risk Factors; D012720:Severity of Illness Index; D012995:Solubility; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood
D052242:Adiponectin; D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; D020738:Leptin; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D011956:Receptors, Cell Surface; D000072483:Placenta Growth Factor; D040281:Vascular Endothelial Growth Factor Receptor-1; D040301:Vascular Endothelial Growth Factor Receptor-2