阿尔法(金融)
平衡
雌激素
雌激素受体
雌激素受体α
细胞生物学
受体
生物
内分泌学
内科学
医学
结构效度
癌症
护理部
乳腺癌
患者满意度
作者
Jason A. Rizo,Kimberly M. Davenport,Wipawee Winuthayanon,Thomas E. Spencer,Andrew M. Kelleher
出处
期刊:iScience
[Elsevier]
日期:2023-08-09
卷期号:26 (9): 107568-107568
被引量:4
标识
DOI:10.1016/j.isci.2023.107568
摘要
Postnatal development of the uterus involves specification of undifferentiated epithelium into uterine-type epithelium. That specification is regulated by stromal-epithelial interactions as well as intrinsic cell-specific transcription factors and gene regulatory networks. This study utilized mouse genetic models of Esr1 deletion, endometrial epithelial organoids (EEO), and organoid-stromal co-cultures to decipher the role of Esr1 in uterine epithelial development. Organoids derived from wild-type (WT) mice developed a normal single layer of columnar epithelium. In contrast, EEO from Esr1 null mice developed a multilayered stratified squamous type of epithelium with basal cells. Co-culturing Esr1 null epithelium with WT uterine stromal fibroblasts inhibited basal cell development. Of note, estrogen treatment of EEO-stromal co-cultures and Esr1 conditional knockout mice increased basal epithelial cell markers. Collectively, these findings suggest that Esr1 regulates uterine epithelium lineage plasticity and homeostasis and loss of ESR1 promotes altered luminal-to-basal differentiation driven by ESR1-mediated paracrine factors from the stroma.
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