Elevated Serum Soluble Vascular Endothelial Growth Factor Receptor 1 (sVEGFR-1) Levels in Women with Preeclampsia

Koga, Kaori; Osuga, Yutaka; Yokosuka, Osamu; Hirota, Yasushi; Ruimeng, Xie; Hirata, Tetsuya; Takeda, Satoru; Yano, Tetsu; Tsutsumi, Osamu; Taketani, Yuji

doi:10.1210/jc.2002-021942

Cited by 364 publications

(224 citation statements)

References 0 publications

Supporting

Mentioning

202

Contrasting

Unclassified

Order By: Relevance

“…[16][17][18] Moreover, recent reports have indicated that the soluble form of the VEGF receptor-1 (sFlt-1) is increased in the placenta and serum of women with PE. [18][19][20][21] Thus, sFlt-1 may act by sequestering free PlGF and free VEGF, thereby preventing interaction between endothelial Median (interquartile range).…”

Section: Discussionmentioning

confidence: 99%

Different profiles of circulating angiogenic factors and adipocytokines between early‐ and late‐onset pre‐eclampsia

Masuyama

Segawa

Sumida

et al. 2010

BJOG

109

View full text Add to dashboard Cite

Objective Circulating angiogenic factors have been shown to be important in the pathophysiology of pre-eclampsia. Blood levels of adipocytokines differ in pre-eclampsia relative to controls and may also play an important role in disease pathogenesis. Differences in the circulating levels of these molecules were compared between matched normotensive controls and women with pre-eclampsia with onset before or at/after 32 weeks, and according to whether the women were of normal weight (18.5 < body mass index < 25) or overweight.Design A cross-sectional study of 110 pregnant Japanese women who visited the Department of Obstetrics and Gynecology, Okayama University Hospital, Okayama, Japan.Setting Tertiary referral centre serving 2000 births.Methods Serum concentrations of soluble fms-like tyrosine kinase 1 (sFlt-1), placental growth factor (PlGF), soluble endoglin (sEng), adiponectin and leptin were measured in women with pre-eclampsia and in normotensive controls matched for age, gestational week, parity and body mass index.Main outcome measures Serum levels of sFlt-1, PlGF, the sFlt-1/ PlGF ratio, sEng, adiponectin and leptin.Results The sFlt-1/PlGF ratio in early-onset pre-eclampsia was significantly higher than that in late-onset pre-eclampsia (112.0 ± 30.2 versus 45.4 ± 43.8, P = 0.037). There was a significant elevation of leptin in both subtypes relative to controls (early: 58.6 ± 18.3 ng/ml versus 26.0 ± 6.7 ng/ml, P = 0.001; late: 39.5 ± 9.2 ng/ml versus 22.0 ± 4.3 ng/ml, P = 0.005), but adiponectin was increased only in late-onset pre-eclampsia (36.5 ± 13.4 lg/ml versus 12.0 ± 4.3 lg/ml, P = 0.003). Significant differences in angiogenic factors and adiponectin were found between normal and overweight women only in late-onset pre-eclampsia.Conclusions These data suggest that there are different profiles of angiogenic factors and adipocytokines between women who develop early-and late-onset pre-eclampsia.

show abstract

Section: Discussionmentioning

confidence: 99%

Different profiles of circulating angiogenic factors and adipocytokines between early‐ and late‐onset pre‐eclampsia

Masuyama

Segawa

Sumida

et al. 2010

BJOG

109

View full text Add to dashboard Cite

show abstract

“…Excess sFlt1 alone, when administered to pregnant rats, induces albuminuria, hypertension, and renal pathologic changes of glomerular endotheliosis by antagonizing circulating VEGF and PlGF and inducing endothelial dysfunction. In addition, circulating levels of free VEGF and free PlGF were decreased in conjunction with elevated sFlt1 in the bloodstream at the time of disease presentation (39,40). More recently, when free PlGF and free VEGF were measured throughout pregnancy, the growth factors were decreased in preeclamptic women well before the onset of clinical disease (46 -48).…”

Section: Circulating Proangiogenic Factors and Their Inhibitorsmentioning

confidence: 99%

New Aspects in the Pathophysiology of Preeclampsia

Davison¹,

Homuth²,

Jeyabalan³

et al. 2004

Journal of the American Society of Nephrology

171

109

View full text Add to dashboard Cite

Abstract. Preeclampsia, the de novo occurrence of hypertension and proteinuria after the 20th week of gestation, continues to exert an inordinate toll on mothers and children alike. Recent clinical trials, new physiologic insights, and novel observations on pathogenesis have altered the thinking about preeclampsia. The mechanisms surrounding relaxin and its effects on the circulation and on matrix metalloproteinases have been elucidated. The growth factor's receptor, fms-like tyrosine kinase 1, has been shown to exist in a soluble form that is able to inactivate vascular endothelial-derived growth factor and human placental growth factor. Compelling evidence has been brought forth suggesting that fms-like tyrosine kinase 1 is a circulating factor that can cause preeclampsia. Preeclamptic women have high circulating levels of asymmetric dimethyl arginine that could account for the generalized endothelial dysfunction observed in preeclampsia. Preeclamptic women also produce novel autoantibodies that may serve to activate angiotensin receptors. These new observations raise the possibility that the treatment of preeclamptic women will soon be improved.The term preeclampsia refers to the new onset of hypertension (Ͼ140/90 mmHg) and proteinuria after 20 wk of gestation in previously normotensive, nonproteinuric women (1). The condition is common and occurs in~5% of pregnancies in the United States and Europe. Eclampsia is a life-threatening complication and is characterized by grand mal seizures. The term comes from the Greek word for lightning. A severe variant of preeclampsia also features hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). This condition occurs iñ 1 per 1000 pregnancies. Predisposing factors are a positive family history, hypertension, diabetes, preexisting renal disease, multiple pregnancies, and a poor obstetric history. Nephrologists are often called on to see preeclamptic women because of the severe BP elevation and renal disease. Thus, new clinical or experimental information on this condition is important information for nephrologists. Preeclampsia and Subsequent Cardiovascular RiskThe relevance of preeclampsia to the offspring is well recognized. Children who are born to preeclamptic mothers commonly have low birth weight, and their subsequent cardiovascular risk has been a vast investigational field. The mother's outcome has attracted less interest. Chesley, the father of modern preeclampsia research, was of the opinion that once the condition was over, the mothers had no greater risk of adverse long-term outcomes than women without preeclampsia from the general population (2). This issue may prove to be the only matter in which Chesley's opinion was erroneous. Several recent studies suggest that the converse is the case. Smith et al. (3) studied the pregnancy complications and the maternal risk of ischemic cardiac death in 129,290 births. They found that delivering an infant with low birth weight for gestational age increased the hazard ratio for ischemic heart disease o...

show abstract

“…It seems that during pregnancy most of the circulating VEGF is bound to sVEGFR-1 produced in high amounts by the placenta [19][20][21]. In preeclampsia, placental production of VEGFR-1 and sVEGFR-1 is likely increased because of low oxygen levels in the placenta.…”

Section: Expression Of Vegf Plgf and Their Receptors In Pregnancies mentioning

confidence: 99%

Fetal growth restriction: a workshop report

et al. 2004

View full text Add to dashboard Cite

Intrauterine growth restriction (IUGR) is associated with significantly increased perinatal morbidity and mortality as well as cardiovascular disease and glucose intolerance in adult life. A number of disorders from genetic to metabolic, vascular, coagulative, autoimmune, as well as infectious, can influence fetal growth by damaging the placenta, leading to IUGR as a result of many possible fetal, placental and maternal disorders. Strict definitions of IUGR and of its severity are needed in order to eventually distinguish among different phenotypes, such as gestational age at onset, degree of growth restriction and presence of hypoxia.This report explores and reviews some of the most recent developments in both clinical and basic research on intrauterine growth restriction, by seeking mechanisms that involve genetic factors, utero-placental nutrient availability and vascular growth factors.New exciting findings on the genomic imprinting defects potentially associated with IUGR, and the placental anomalies associated with the decreased nutrient transport are summarized. Moreover, recent data on angiogenic growth factors as well as new information arising from application of gene chip technologies are discussed.

show abstract

Elevated Serum Soluble Vascular Endothelial Growth Factor Receptor 1 (sVEGFR-1) Levels in Women with Preeclampsia

Cited by 364 publications

References 0 publications

Different profiles of circulating angiogenic factors and adipocytokines between early‐ and late‐onset pre‐eclampsia

Different profiles of circulating angiogenic factors and adipocytokines between early‐ and late‐onset pre‐eclampsia

New Aspects in the Pathophysiology of Preeclampsia

Fetal growth restriction: a workshop report

Contact Info

Product

Resources

About