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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [CUT&RUN]

ABSTRACT: TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [CUT&RUN]

PROVIDER: PRJNA875482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21381086_1.fastq.gz	Fastqsanger.gz
	SRR21381086_2.fastq.gz	Fastqsanger.gz
	SRR21381087_1.fastq.gz	Fastqsanger.gz
	SRR21381087_2.fastq.gz	Fastqsanger.gz
	SRR21381088_1.fastq.gz	Fastqsanger.gz

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

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

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TGFβ signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration [CUT&RUN]

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

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The effect of obesity on uterine receptivity is mediated by endometrial extracellular vesicles that control human endometrial stromal cell decidualization and trophoblast invasion

Project description:The objectives of the present study were to determine whether obesity impacts human decidualization and the endometrial control of trophoblast invasion (both of which are required for embryo implantation) and evaluate the potential involvement of endometrial extracellular vesicles (EVs) in the regulation of these physiological processes. Using primary human cell cultures, we first demonstrated that obesity is associated with significantly lower in vitro decidualization of endometrial stromal cells (ESCs). We then showed that the trophoblastic cell line’s invasive ability was greater in the presence of conditioned media from cultures of ESCs from obese women. Using mass-spectrometry-based quantitative proteomics, we found that EVs isolated from uterine supernatants of biopsies from obese women (vs. nonobese women) presented a molecular signature focused on cell remodeling and angiogenesis. Lastly, the results of functional assays indicated that supplementation of the culture medium with EVs from nonobese women can rescue (at least in part) the defect in in vitro decidualization described in ESCs from obese women. Lastly, the addition of endometrial EVs from obese women (vs. nonobese women) was associated with significantly greater invasive activity by HTR-8/SVneo cells. In conclusion, our results provided new insights into the endometrial EVs’ pivotal role in the poor uterine receptivity observed in obese women.

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