First published October 1, 2013 - More info
During human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4%–8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) and, in some patients, fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously, we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, we cultured CTBs isolated from PE and control placentas for 48 hours, enabling differentiation and invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation, including upregulation of
Yan Zhou, Matthew J. Gormley, Nathan M. Hunkapiller, Mirhan Kapidzic, Yana Stolyarov, Victoria Feng, Masakazu Nishida, Penelope M. Drake, Katherine Bianco, Fei Wang, Michael T. McMaster, Susan J. Fisher
Original citation: J Clin Invest. 2013;123(7):2862–2872. doi:10.1172/JCI66966.
Citation for this corrigendum: J Clin Invest. 2013;123(10):4541. doi:10.1172/JCI72817.
During the preparation of this manuscript, support from one NIH grant was omitted from the Acknowledgments. The correct Acknowledgments section is below.
We are grateful to Jean Perry, Julie de la Garza, and Brittni Johnson for patient recruitment. We also thank Mari-Paule Thiet, the UCSF Maternal-Fetal Medicine Division, and The Women’s Option Center at San Francisco General Hospital for invaluable help in obtaining the placental samples that made this study possible. Finally, we are grateful to the study participants. This work was supported by NIH grants HD030367 and HD046744 and the UCSF Department of Obstetrics, Gynecology and Reproductive Sciences.
The authors regret the error.