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The Circulating Proangiogenic Factors CYR61 (CCN1) and NOV (CCN3) Are Significantly Decreased in Placentae and Sera of Preeclamptic Patients

Institute of Anatomy, University Hospital Essen, Essen, Germany, alexandra.gellhaus{at}uni-essen.de

Markus Schmidt, MD

Department of Gynecology and Obstetrics, University Hospital Essen, Essen, Germany

Caroline Dunk, PhD

Department of Obstetrics and Gynecology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada

Stephen J. Lye, PhD

Department of Obstetrics and Gynecology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada

Elke Winterhager, PhD

Institute of Anatomy, University Hospital Essen, Essen, Germany

It is thought that preeclampsia results from a shallow invasion of the extravillous trophoblast into the decidua and maternal vessels, which in turn leads to hypoxia and uteroplacental insufficiency. Here, the authors focus on the expression of the proangiogenic secreted molecules CYR61 (CCN1) and NOV (CCN3) in human placentae during normal pregnancy compared with preeclamptic placentae. CYR61 and NOV are strongly expressed in endothelial cells as well as in the extravillous trophoblast, with increasing levels during placental development. Interestingly, the authors found significantly decreased levels in early preeclamptic placentae compared with matched controls. Whereas both CYR61 and NOV proteins are present at constant high levels in the sera of nonpregnant and pregnant women, in the sera of patients with early-onset preeclampsia, levels were significantly reduced. The authors suggest that the reduction of both CCN molecules in preeclampsia could be 1 reason underlying the failure of uterine vascular remodeling. Moreover, their low maternal serum levels could serve as biomarkers for early diagnosis of this disease.

Key Words: Angiogenesis • cystein-rich 61 protein • nephroblastoma overexpressed protein • placenta • preeclampsia.

Reproductive Sciences, Vol. 14, No. 8 suppl, 46-52 (2007)
DOI: 10.1177/1933719107309816


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