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Syncytin, a novel human endogenous retroviral gene in human placenta: evidence for its dysregulation in preeclampsia and HELLP syndrome.
American Journal of Obstetrics and Gynecology 2002 Februrary
OBJECTIVE: A novel human endogenous retroviral element, designated as syncytin, has been suggested as a contributor to normal placental architecture, especially in the fusion processes of cytotrophoblasts to syncytiotrophoblasts. We tested the hypothesis of whether the gene expression of syncytin may be altered in cases with placental dysfunction such as preeclampsia or HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome.
STUDY DESIGN: We included 30 women with normal pregnancies, 16 with preeclampsia, and 6 with HELLP syndrome. After delivery, messenger ribonucleic acids (mRNA) of syncytin, glyceraldehyde-3-phosphate dehydrogenase and beta-actin were analyzed in placental villi with use of quantitative real-time polymerase chain reaction.
RESULTS: In placental villi, syncytin mRNA/beta-actin mRNA and syncytin mRNA/glyceraldehyde-3-phosphate dehydrogenase mRNA ratios were lower in patients with preeclampsia (P <.05) or HELLP syndrome than in healthy control subjects.
CONCLUSION: A reduced placental expression of syncytin may contribute to altered cell fusion processes in placentogenesis and disturbed placental function in hypertensive disorders of pregnancy.
STUDY DESIGN: We included 30 women with normal pregnancies, 16 with preeclampsia, and 6 with HELLP syndrome. After delivery, messenger ribonucleic acids (mRNA) of syncytin, glyceraldehyde-3-phosphate dehydrogenase and beta-actin were analyzed in placental villi with use of quantitative real-time polymerase chain reaction.
RESULTS: In placental villi, syncytin mRNA/beta-actin mRNA and syncytin mRNA/glyceraldehyde-3-phosphate dehydrogenase mRNA ratios were lower in patients with preeclampsia (P <.05) or HELLP syndrome than in healthy control subjects.
CONCLUSION: A reduced placental expression of syncytin may contribute to altered cell fusion processes in placentogenesis and disturbed placental function in hypertensive disorders of pregnancy.
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