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

被引:29
作者
Gellhaus A. [1 ]
Schmidt M. [2 ]
Dunk C. [3 ]
Lye S.J. [3 ]
Winterhager E. [4 ]
机构
[1] Institute of Anatomy, University Hospital Essen, Hufelandstr 55, Essen
[2] University Hospital Essen, Essen
[3] Department of Obstetrics and Gynecology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto
关键词
Angiogenesis; cystein-rich; 61; protein; nephroblastoma overexpressed protein; placenta; preeclampsia;
D O I
10.1177/1933719107309816
中图分类号
学科分类号
摘要
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. © 2007 by the Society for Gynecologic Investigation.
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页码:46 / 52
页数:6
相关论文
共 21 条
[1]  
Myatt L., Role of placenta in preeclampsia, Endocrine., 19, 1, pp. 103-111, (2002)
[2]  
Bdolah Y., Karumanchi S.A., Sachs B.P., Recent advances in understanding of preeclampsia, Croat Med J., 46, 5, pp. 728-736, (2005)
[3]  
Sibai B., Dekker G., Kupferminc M., Pre-eclampsia, Lancet., 365, pp. 785-799, (2005)
[4]  
Redman C.W., Sargent I.L., Latest advances in understanding preeclampsia, Science., 308, 5728, pp. 1592-1594, (2005)
[5]  
Schmidt M., Gellhaus A., Kasimir-Bauer S., Et al., Angiogenic factors during pregnancy: Indicators of preeclampsia, Geburtshilfe und Frauenheilkunde, 67, pp. 217-227, (2007)
[6]  
Zhou Y., Damsky C.H., Chiu K., Et al., Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts, J Clin Invest., 91, 3, pp. 950-960, (1993)
[7]  
Lim K.H., Zhou Y., Janatpour M., Et al., Human cytotrophoblast differentiation/invasion is abnormal in pre-eclampsia, Am J Pathol., 151, 6, pp. 1809-1818, (1997)
[8]  
Zhou Y., McMaster M., Woo K., Et al., Vascular endothelial growth factor ligands and receptors that regulate human cytotrophoblast survival are dysregulated in severe preeclampsia and hemolysis, elevated liver enzymes, and low platelets syndrome, Am J Pathol., 160, 4, pp. 1405-1423, (2002)
[9]  
Maynard S.E., Min J.Y., Merchan J., Et al., Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia, J Clin Invest., 111, 5, pp. 649-658, (2003)
[10]  
Venkatesha S., Toporsian M., Lam C., Et al., Soluble endoglin contributes to the pathogenesis of preeclampsia, Nat Med., 12, 6, pp. 642-649, (2006)