Endothelial Cells in Physiology and in the Pathophysiology of Vascular Disorders

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants.

Preeclampsia: an excessive maternal inflammatory response to pregnancy.

Many mammalian viruses have acquired genes from their hosts during their evolution1. The rationale for these acquisitions is usually quite clear: the captured genes are subverted to provide a selective advantage to the virus. Here we describe the opposite situation, where a viral gene has been sequestered to serve an important function in the physiology of a mammalian host. This gene, encoding a protein that we have called syncytin, is the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W2. We find that the major sites of syncytin expression are placental syncytiotrophoblasts, multinucleated cells that originate from fetal trophoblasts. We show that expression of recombinant syncytin in a wide variety of cell types induces the formation of giant syncytia, and that fusion of a human trophoblastic cell line expressing endogenous syncytin can be inhibited by an anti-syncytin antiserum. Our data indicate that syncytin may mediate placental cytotrophoblast fusion in vivo, and thus may be important in human placental morphogenesis.

Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis.

W B Robertson

Papers

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants.

The role of the spiral arteries in the pathogenesis of preeclampsia.

The physiological response of the vessels of the placental bed to normal pregnancy

Uteroplacental arterial changes related to interstitial trophoblast migration in early human pregnancy

Review article: Trophoblast invasion and the establishment of haemochorial placentation in man and laboratory animals