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Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis [MSCTAC]

ABSTRACT: Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis [MSCTAC]

PROVIDER: PRJNA432238 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6653334.fastq.gz	Fastqsanger.gz
	SRR6653335.fastq.gz	Fastqsanger.gz
	SRR6653336.fastq.gz	Fastqsanger.gz
	SRR6653337.fastq.gz	Fastqsanger.gz
	SRR6653338.fastq.gz	Fastqsanger.gz

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Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis

Project description:Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis

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Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis [Axin2beta]

Project description:Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis [Axin2beta]

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Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Microarray Expression]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. Using gene microarray profiling, we show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

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Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Histone ChIP]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. We show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. We also identify an essential requirement for TACs in maintaining the mesenchymal stem cells, indicative of a positive feedback mechanism. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

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Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Ring1b ChIP]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. We show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. We also identify an essential requirement for TACs in maintaining the mesenchymal stem cells, indicative of a positive feedback mechanism. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

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Bi-directional epithelial-mesenchymal crosstalk provides self-sustaining pro-fibrotic signals in pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic lung disease with a median survival of 2-4 years. Injury to and/or dysfunction of alveolar epithelium are strongly implicated in IPF disease initiation, but what factors determine why fibrosis progresses rather than normal tissue repair occurs remain poorly understood. We previously demonstrated that ZEB1-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments TGF-β-induced profibrogenic responses in underlying lung fibroblasts by paracrine signalling. Here we investigated bi-directional epithelial-mesenchymal crosstalk and its potential to drive fibrosis progression. RNA sequencing (RNA-seq) of lung fibroblasts exposed to conditioned media from ATII cells undergoing RAS-induced EMT identified many differentially expressed genes including those involved in cell migration and extracellular matrix (ECM) regulation. We confirmed that paracrine signalling between AS-activated ATII cells and fibroblasts augmented fibroblast recruitment and demonstrated that this involved a ZEB1-tissue plasminogen activator (tPA) axis. In a reciprocal fashion, paracrine signalling from TGF-β-activated lung fibroblasts or IPF fibroblasts induced RAS activation in ATII cells, at least partially via the secreted protein, SPARC. Together these data identify that aberrant bi-directional epithelial-mesenchymal crosstalk in IPF drives a chronic feedback loop that maintains a wound-healing phenotype and provides self-sustaining pro-fibrotic signals.

2021-08-19 | PXD025821 | Pride

Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Bi-directional interaction between mesenchymal stem cells and transit amplifying cells in mesenchymal tissue homeostasis [Axin2beta]

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