Syncytiotrophoblast Markers Are Downregulated in Placentas from Idiopathic Stillbirths

特发性死产导致胎盘合体滋养层细胞标志物下调

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作者:Sara Vasconcelos, Ioannis Moustakas, Miguel R Branco, Susana Guimarães, Carla Caniçais, Talia van der Helm, Carla Ramalho, Cristina Joana Marques, Susana M Chuva de Sousa Lopes, Sofia Dória

Abstract

The trophoblast cells are responsible for the transfer of nutrients between the mother and the foetus and play a major role in placental endocrine function by producing and releasing large amounts of hormones and growth factors. Syncytiotrophoblast cells (STB), formed by the fusion of mononuclear cytotrophoblasts (CTB), constitute the interface between the foetus and the mother and are essential for all of these functions. We performed transcriptome analysis of human placental samples from two control groups-live births (LB), and stillbirths (SB) with a clinically recognised cause-and from our study group, idiopathic stillbirths (iSB). We identified 1172 DEGs in iSB, when comparing with the LB group; however, when we compared iSB with the SB group, only 15 and 12 genes were down- and upregulated in iSB, respectively. An assessment of these DEGs identified 15 commonly downregulated genes in iSB. Among these, several syncytiotrophoblast markers, like genes from the PSG and CSH families, as well as ALPP, KISS1, and CRH, were significantly downregulated in placental samples from iSB. The transcriptome analysis revealed underlying differences at a molecular level involving the syncytiotrophoblast. This suggests that defects in the syncytial layer may underlie unexplained stillbirths, therefore offering insights to improve clinical obstetrics practice.

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