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The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury byparacrine signaling

ABSTRACT: The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury byparacrine signaling

PROVIDER: PRJNA1019662 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26134774_1.fastq.gz	Fastqsanger.gz
	SRR26134774_2.fastq.gz	Fastqsanger.gz
	SRR26134775_1.fastq.gz	Fastqsanger.gz
	SRR26134775_2.fastq.gz	Fastqsanger.gz
	SRR26134776_1.fastq.gz	Fastqsanger.gz

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The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury byparacrine signaling

Project description:Paracrine signals play pivotal roles in organ homeostasis. Mesenchymal stromal cells (MSCs) play a key role in regulating epithelium homeostasis in the intestine while their paracrine effects are poorly characterized. Here, we identified prostaglandin E2 (PGE2) secreted by cyclooxygenase (COX)-expressing MSCs as a vital factor to maintain the intestinal mucosal barrier. We found that MSCs-induced organoid swelling through paracrine effect in vitro, a process due to enhanced water adsorption and is mediated by the COX-PGE2-EP4 axis. To further explore the regulatory effect of this axis on the intestinal epithelial barrier in vivo, we established the conditional knockout mouse model to specifically delete COX in MSCs and found that PGE2 reduction downregulated the gene Muc2 and induced a gastric metaplasia-like phenotype. Moreover, PGE2 defects increased the susceptibility of intestinal epithelium to colitis. Our study uncovers the paracrine signaling of COX-expressing MSCs in intestinal mucosal barrier maintenance, providing a basis for understanding the role of mesenchymal cells in the psychophysiology function of the intestine.

2023-09-26 | GSE243704 | GEO

The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury by paracrine signaling.

| S-EPMC10423710 | biostudies-literature

Correction: The cyclooxygenase-expressing mesenchyme resists intestinal epithelial injury by paracrine signaling.

Project description: Not available

| S-EPMC10587043 | biostudies-literature

Deletion of Tfam in Prx1-Cre expressing limb mesenchyme results in spontaneous bone fractures

Project description:Deletion of Tfam in Prx1-Cre expressing limb mesenchyme results in spontaneous bone fractures

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Primary mouse embryonic palatal mesenchyme LC-MS/MS

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2019-06-04 | PXD000779 | Pride

Hepatocytes cyclooxygenase-2 deficiency improves liver injury via inhibition of endoplasmic reticulum stress and epithelial-mesenchymal transition

Project description:The mechanism underlying the loss of normal liver tissues in liver cirrhosis, mainly hepatocytes, is not well-characterized. Endoplasmic reticulum (ER) stress-induced cell death has emerged as a potential mechanism for chronic liver diseases. We have previously demonstrated that cyclooxygenase-2 (COX-2) is closely related to the progress of liver cirrhosis. In this study, we aimed to verify whether hepatocytes COX-2 deficiency could protect liver injury via inducing ER stress in liver cirrhosis.

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Transcription profiling of mouse E18.5 intestinal mesenchyme treated with Sonic or Indian hedgehog ligand to identify targets regulated by Hedgehog signaling

Project description:Epithelial Hedgehog (Hh) ligands regulate several aspects of fetal intestinal organogenesis and emerging data implicate the Hh pathway in inflammatory signaling in adult colon. We investigated the effects of chronic Hh inhibition in vivo and profiled molecular pathways acutely modulated by Hh signaling in the intestinal mesenchyme. Experiment Overall Design: E18.5 intestinal mesenchyme was isolated and cultured. Mesenchyme was treated with Sonic (Shh) or Indian (Ihh) hedgehog ligand or Vehicle (control) acutely to identify targets regulated by Hh signaling in intestinal mesenchyme.

2009-11-10 | E-GEOD-17840 | biostudies-arrayexpress

Transcriptome analysis of embryonic mesenchyme

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Transcriptional profiling of inductive prostatic mesenchyme

Project description:Background: The mesenchymal compartment plays a key role in organogenesis and cells within the mesenchyme/stroma are a source of potent molecules that control epithelia during development and tumourigenesis. We have used Serial Analysis of Gene Expression (SAGE) to profile a key subset of prostatic mesenchyme that regulates prostate development and is enriched for growth-regulatory molecules. Results: SAGE libraries were made of prostatic inductive mesenchyme (VMP) and the complete prostatic rudiment (including inductive mesenchyme, epithelium and smooth muscle; VSU). By comparing these two SAGE libraries we generated a list of 219 transcripts that were enriched or specific to inductive mesenchyme and which may act as mesenchymal regulators of organogenesis and tumourigenesis. Conclusions: The use of a precisely defined subset of cells, and a back-comparison approach, allowed us to identify rare mRNAs that might be overlooked using other approaches. Keywords: SAGE, gene profiling Two SAGE libraries were prepared and compared to each other. The VMP forms a subset of the VSU.

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