The diversity of trophoblast cells and niches of placenta accreta spectrum disorders revealed by single-cell RNA sequencing.
Jingmei Ma, Yawei Liu, Zhirong Guo, Run Sun, Xinrui Yang, Weiran Zheng, Yongdan Ma, Yin Rong, Hongmei Wang, Huixia Yang, Zhenyu Xiao
Author Information
Jingmei Ma: State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Yawei Liu: State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Zhirong Guo: Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Run Sun: State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Xinrui Yang: Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Weiran Zheng: Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Yongdan Ma: Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Yin Rong: State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Hongmei Wang: State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Huixia Yang: Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Zhenyu Xiao: State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
中文译文
English
Placenta accreta spectrum disorders (PAS) are severe pregnancy complications that occur when extravillous trophoblast cells (EVTs) invade beyond the uterine inner myometrium and are characterized by hypervascularity on prenatal ultrasound and catastrophic postpartum hemorrhage. The potential mechanisms remain incompletely understood. With single-cell RNA-sequencing analysis on the representative invasive parts and the normal part obtained from the same PAS placenta, we profiled the pathological landscape of invasive PAS placenta and deciphered an intensified differentiation pathway from progenitor cytotrophoblasts (CTBs) to EVTs and CTBs. In the absence of the decidua, the invasive trophoblasts of various differentiation states interacted with and maternal stromal cells. The PAS-associated hypervascularity might be due to the enhanced crosstalk of trophoblasts, stromal cells and vascular endothelial cells. Finally, we presented an immune microenvironmental landscape of invasive PAS. The pathogenesis of PAS could be further explored with current resources for future targeted translational studies.
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