Endoglin/CD105 is a transmembrane co-receptor that facilitates the binding of TGF-beta 1 or -beta 3 to TGF-beta RII and the recruitment of the type I receptor ALK-1. Endoglin expression is upregulated in endothelial cells and syncytiotrophoblasts during development of the placenta in early pregnancy. Preeclampsia, a condition defined by increased blood pressure and proteinuria, occurs in 5% of pregnancies worldwide. This common and potentially life-threatening complication of pregnancy increasingly appears to be caused by placental insufficiency. Recently, it has been shown that increases in the soluble form of endoglin are exaggerated during and, significantly, prior to the onset of preeclamptic symptoms.1
The Endoglin/CD105 Quantikine ELISA Kit (Catalog # DNDG00) is a reliable means for detecting endoglin in biological fluids. Researchers from Harvard Medical School have recently used the kit to demonstrate a two- and three-fold endoglin increase in preterm and term pregnancy, respectively, compared to non-pregnant states.1 Significantly, mild preeclampsia, severe preeclampsia, and HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) are accompanied by a further three-, five-, and ten-fold increase in circulating endoglin, respectively, as detected by the Quantikine Kit. These elevated endoglin levels closely parallel increases in sVEGF R1/Flt-1 also assessed using R&D Systems Quantikine ELISA Kit (Catalog # DVR100B; Figure 1). The role of the placenta is demonstrated by the rapid decrease in the levels of endoglin 48 hours after delivery (Figure 2).
Serum or plasma placental growth factor (PlGF) and soluble VEGF R1 (sVEGF R1) also increase during normal pregnancy. In preeclampsia, the circulating PlGF increase is attenuated while increases in both sVEGF R1 and endoglin are exaggerated. An additional report by the Harvard group has demonstrated that the combination of high sVEGF R1/PlGF ratio with high endoglin gives an adjusted odds ratio greater than 30-fold for the subsequent development of either preterm or term preeclampsia.2 The combination of the two values is more predictive than either value alone.
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Figure 1. ELISA results for endoglin and sVEGF R1/Flt-1 in sera of individuals with varying degrees of preeclampsia (PE), control pregnancies, and four nonpregnant healthy volunteers. *P < 0.05 compared to preterm controls, #P < 0.05 compared to severe preeclampsia. HELLP; hemolysis, elevated liver enzymes, low platelets. Figure adapted with permission from Nature Medicine.1 |
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Figure 2. ELISA results for endoglin in a subset of pregnant individuals (normal, n = 6; preeclampsia, n = 11) with blood drawn before (0–12 h) or after (48 h) delivery. *P < 0.05 as compared to pre-delivery samples. Figure adapted with permission from Nature Medicine.1 |
References
- Venkatesha, S. et al. (2006) Soluble endoglin contributes to the pathogenesis of preeclampsia. Nat. Med. 12:642.
- Levine, R. J. et al. (2006) Soluble endoglin and other circulating antiangiogenic factors in preeclampsia. N. Engl. J. Med. 355:992.