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Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases [scRNA-seq]

ABSTRACT: Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases [scRNA-seq]

PROVIDER: PRJNA842769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19424366_1.fastq.gz	Fastqsanger.gz
	SRR19424366_2.fastq.gz	Fastqsanger.gz
	SRR19424367_1.fastq.gz	Fastqsanger.gz
	SRR19424367_2.fastq.gz	Fastqsanger.gz
	SRR19424368_1.fastq.gz	Fastqsanger.gz

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Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases.

Project description:Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases.

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Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases [scRNA-seq]

Project description:Diseases of the biliary epithelium (cholangiopathies) are an important cause of morbidity and mortality. Their pathogenesis and treatment remain unclear, in part because of the lack of disease models relevant to humans. 3D biliary organoids hold great promise, however the inaccessibility of their apical pole, and the presence of extracellular matrix (EBM) limit their experimental application. Here we show that when b integrin signaling is inhibited, either by removing the EMC or using blocking antibodies, biliary organoids revert their polarity and expose the apical membrane. Functional, immunohistochemical and TEM studies, along with bulk and single cell transcriptomic demonstrate that organoids in this novel 3D configuration, are less heterogeneous, show increased biliary differentiation, and decreased expression of stem cell markers. This model can be used to study bile transport, interactions with microbial agents, epithelial permeability, cross-talk with other liver and immune cell types and the effect of matrix changes on the biliary epithelium.

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Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases [bulk RNA-seq]

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Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases [bulk RNA-seq]

Project description:Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases [bulk RNA-seq]

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Cell-matrix interactions control biliary organoids polarity,architecture and differentiation and can be exploited to improve modelling of biliary diseases.

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2023-09-21 | GSE204960 | GEO

Biliary organoids uncover delayed epithelial development and barrier function in biliary atresia.

Project description:Background: RNASeq was performed on organoids derived from livers of normal healthy donors and patients with biliary atresia to characterize transcriptomic signatures. Methods: Organoids generated from livers of normal healthy donors and patients with biliary atresia were cultured either in expansion (undifferentiated: 3 NCOs and 11 BACOs) or differentiation medium (differentiated: 3 BACOs). Liver tissues obtained from deceased-donor subjects served as normal controls (N=3). Total RNA was isolated from organoids and liver biopsy tissue specimens. Results: Organoids from patients with biliary atresia showed abnormal cell polarity, loss of tight junctions, increased permeability and decreased expression of genes related to epidermal growth factor (EGF)- and fibroblast growth factor 2 (FGF2)-signaling. When treated with EGF+FGF2, biliary atresia organoids expressed differentiation and functional markers with restored cell polarity. Conclusion: Organoids from biliary atresia are viable and have evidence of halted epithelial development. The induction of developmental markers, improved cell‐cell junction, and decreased epithelial permeability by EGF and FGF2 identifies potential strategies to promote epithelial maturation and function.

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Project description:Restitution of the extrahepatic biliary luminal epithelium in cholangiopathies is poorly understood. Prominin-1 (Prom1) is a key component of epithelial ciliary body of stem/progenitor cells. Given that intrahepatic Prom1-expressing progenitor cells undergo cholangiocyte differentiation, we hypothesized that Prom1 may promote restitution of the extrahepatic bile duct (EHBD) epithelium following injury. Utilizing various murine biliary injury models, we identified Prom1-expressing cells in the peribiliary glands (PBGs) of the EHBD. These Prom1-expressing cells are progenitor cells which give rise to cholangiocytes as part of the normal maintenance of the EHBD epithelium. Following injury, these cells proliferate significantly more rapidly to re-populate the biliary luminal epithelium. Null mutation of Prom1 leads to significantly more than ten-fold dilated PBGs following rhesus rotavirus-mediated biliary injury. Cultured organoids derived from Prom1 knockout mice are comprised of biliary progenitor cells with altered apical-basal cellular polarity, significantly fewer and shorter cilia, and decreased organoid proliferation dynamics consistent with impaired cell motility. We, therefore, conclude that Prom1 is involved in biliary epithelial restitution following biliary injury in part through its role in supporting cell polarity.

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