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NOTCH3信号通路控制人类滋养层干细胞的扩增和分化。

NOTCH3 signalling controls human trophoblast stem cell expansion and differentiation.

作者信息

Dietrich Bianca, Kunihs Victoria, Lackner Andreas I, Meinhardt Gudrun, Koo Bon-Kyoung, Pollheimer Jürgen, Haider Sandra, Knöfler Martin

机构信息

Placental Development Group, Medical University of Vienna, A-1090 Vienna, Austria.

Maternal-Fetal Immunology Group, Department of Obstetrics and Gynecology, Reproductive Biology Unit, Medical University of Vienna, A-1090 Vienna, Austria.

出版信息

Development. 2023 Nov 15;150(22). doi: 10.1242/dev.202152. Epub 2023 Nov 16.

Abstract

Failures in growth and differentiation of the early human placenta are associated with severe pregnancy disorders such as pre-eclampsia and fetal growth restriction. However, regulatory mechanisms controlling development of placental epithelial cells, the trophoblasts, remain poorly elucidated. Using trophoblast stem cells (TSCs), trophoblast organoids (TB-ORGs) and primary cytotrophoblasts (CTBs) of early pregnancy, we herein show that autocrine NOTCH3 signalling controls human placental expansion and differentiation. The NOTCH3 receptor was specifically expressed in proliferative CTB progenitors and its active form, the nuclear NOTCH3 intracellular domain (NOTCH3-ICD), interacted with the transcriptional co-activator mastermind-like 1 (MAML1). Doxycycline-inducible expression of dominant-negative MAML1 in TSC lines provoked cell fusion and upregulation of genes specific for multinucleated syncytiotrophoblasts, which are the differentiated hormone-producing cells of the placenta. However, progenitor expansion and markers of trophoblast stemness and proliferation were suppressed. Accordingly, inhibition of NOTCH3 signalling diminished growth of TB-ORGs, whereas overexpression of NOTCH3-ICD in primary CTBs and TSCs showed opposite effects. In conclusion, the data suggest that canonical NOTCH3 signalling plays a key role in human placental development by promoting self-renewal of CTB progenitors.

摘要

早期人类胎盘生长和分化异常与子痫前期和胎儿生长受限等严重妊娠疾病相关。然而,控制胎盘上皮细胞(即滋养层细胞)发育的调控机制仍不清楚。利用早孕的滋养层干细胞(TSCs)、滋养层类器官(TB-ORGs)和原代细胞滋养层细胞(CTBs),我们在此表明自分泌NOTCH3信号控制人类胎盘的扩张和分化。NOTCH3受体在增殖性CTB祖细胞中特异性表达,其活性形式,即核内NOTCH3细胞内结构域(NOTCH3-ICD),与转录共激活因子主调控样蛋白1(MAML1)相互作用。在TSC系中强力霉素诱导表达显性负性MAML1会引发细胞融合,并上调多核合体滋养层细胞特异性基因的表达,多核合体滋养层细胞是胎盘分化产生激素的细胞。然而,祖细胞的扩增以及滋养层干细胞特性和增殖的标志物受到抑制。因此,抑制NOTCH3信号会减少TB-ORGs的生长,而在原代CTBs和TSCs中过表达NOTCH3-ICD则显示出相反的效果。总之,数据表明经典NOTCH3信号通过促进CTB祖细胞的自我更新在人类胎盘发育中起关键作用。

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