SDF–1 is elevated in preeclampsia

OBJECTIVES: Stromal cell derived factor–1 (SDF–1) is involved in denovo blood vessel formation, a key process in placental development. Dysregulation of placental angiogenesis in early pregnancy is thought to be the underlying cause of preeclampsia (PE). We hypothesized that SDF–1 is dysregulated in PE and tested this hypothesis by determining the placental expression pattern of SDF–1 in placentas and maternal SDF–1 blood levels in both normal and PE pregnancies.

Methods: We performed case-control studies comparing SDF–1 expression by immuno-localization in placental tissue samples and measured SDF–1 levels by ELISA in maternal blood of women with preeclampsia and healthy controls. Placental tissue samples were obtained after delivery (n=16). Blood was collected at the time of clinical preeclampsia (n=14), before onset of any symptoms of preeclampsia (n=20; at 20 weeks of gestation) and from gestation matched healthy controls (n=14 and 20, respectively).

Results: We observed increased SDF–1 expression by syncytiotrophoblasts in preeclamptic tissue. Furthermore, in subjects with preeclampsia there was a significant increase of SDF–1 concentration in the maternal blood at the time of the disease (P=0.01) and in early pregnancy at 20 weeks of gestation (P=0.04).

Conclusion: Our data suggest that the syncytiotrophoblast layer of the placenta contributes to SDF–1 concentrations in the maternal blood in preeclampsia and that elevated concentrations of SDF–1 at 20 weeks of gestation might play a role in the pathogenesis of preeclampsia. These findings support the hypothesis that an imbalance of angiogenic factors contributes to the development of preeclampsia.