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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration

ABSTRACT: TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration

PROVIDER: PRJNA875479 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21381105_1.fastq.gz	Fastqsanger.gz
	SRR21381105_2.fastq.gz	Fastqsanger.gz
	SRR21381106_1.fastq.gz	Fastqsanger.gz
	SRR21381106_2.fastq.gz	Fastqsanger.gz
	SRR21381107_1.fastq.gz	Fastqsanger.gz

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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [RNA-Seq]

Project description:TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [RNA-Seq]

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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [RNA-Seq]

Project description:In this study, we define the epithelial-specific contribution of SMAD2/3 to endometrial function by conditionally ablating the Smad2 and Smad3 transcription factors using Lactoferrin-iCre (Ltf-cre). Using epithelial organoid cultures from the endometrium, we uncover the signaling mechanisms downstream of TGFβ that control endometrial cell regeneration and are critical for endometrial regeneration and homeostasis.

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Estrogen receptor alpha regulates uterine epithelial lineage specification and homeostasis

Project description: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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Project description:The regenerative potential of the endometrium is attributed to endometrial stem cells; however, the signaling pathways controlling its regenerative potential remain obscure. In this study, genetic mouse models and endometrial organoids are used to demonstrate that SMAD2/3 signaling controls endometrial regeneration and differentiation. Mice with conditional deletion of SMAD2/3 in the uterine epithelium using Lactoferrin-iCre develop endometrial hyperplasia at 12-weeks and metastatic uterine tumors by 9-months of age. Mechanistic studies in endometrial organoids determine that genetic or pharmacological inhibition of SMAD2/3 signaling disrupts organoid morphology, increases the glandular and secretory cell markers, FOXA2 and MUC1, and alters the genome-wide distribution of SMAD4. Transcriptomic profiling of the organoids reveals elevated pathways involved in stem cell regeneration and differentiation such as the bone morphogenetic protein (BMP) and retinoic acid signaling (RA) pathways. Therefore, TGFβ family signaling via SMAD2/3 controls signaling networks which are integral for endometrial cell regeneration and differentiation.

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