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GLI1+ mesenchymal stromal cells modulate epithelial metaplasia in lung fibrosis

ABSTRACT: GLI1+ mesenchymal stromal cells modulate epithelial metaplasia in lung fibrosis

PROVIDER: PRJNA588064 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10408695.fastq.gz	Fastqsanger.gz
	SRR10408697.fastq.gz	Fastqsanger.gz
	SRR10408698.fastq.gz	Fastqsanger.gz

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GLI1+ mesenchymal stromal cells modulate epithelial metaplasia in lung fibrosis

Project description:A single-cell transcriptional analysis was performed on GLI1+ stromal cells from the adult murine lung during homeostasis and after fibrotic injury. The goal is to understand the role of GLI1+ stromal cells in lung fibrosis and repair. Whole adult murine lung tissue from two samples were separately dissociated to single cells and subjected to fluorescence activated cell sorting (FACS) to select all live GLI1+ cells. One sample was treated with bleomycin to induce fibrosis and the other was treated with saline as a control. The single cell RNA-sequencing library was generated separately for the bleomycin and saline-treated samples. Cells were sequenced at a depth of ~70,000 reads/cell. We captured approximately 17,700 cells with a median of 2,400 genes detected per cell utilizing a droplet-based barcoding approach to capture single cells for RNA sequencing. After bleomycin-induced fibrosis, we identified a novel "myofibroblast" subset of GLI1 cells that contribute to injury and repair. Injured GLI1 cells also reveal dysregulation in key developmental pathways, including BMP signaling, that contribute to metaplastic repair after fibrotic injury.

2020-08-17 | GSE140032 | GEO

Expression data from 6-month Helicobacter felis-infected WT and Gli1-/- mouse stomachs

Project description:Gli1 is necessary for the progression from chronic gastric inflammation to metaplasia in the stomach. We therefore compared the expression patterns between 6-month H. felis infected WT and Gli1-/- stomachs. Pooled tissue from the gastric fundi of 3 mice per group. Groups are WT, WT + H. felis (6 months), Gli1-/-, and Gli1-/- +H. felis (6 months). All the infected and control mice were obtained from the same experiment.

2013-01-24 | E-GEOD-43693 | biostudies-arrayexpress

Analysis of mRNA from Gli1 expressing stromal cells of mice given SAG21k versus vehicle

Project description:Comparison of mRNA expression from FACS isolated Gli1 expressing stromal cells from mice given SAG21k versus vehicle

2016-10-21 | GSE88994 | GEO

Expression data from 6-month Helicobacter felis-infected WT and Gli1-/- mouse stomachs

2013-01-24 | GSE43693 | GEO

Gli1+ cells in bone marrow fibrosis

Project description:Gli1+ cells as a driver and key target in bone marrow fibrosis

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Macrophages modulate fibrosis during newt lens regeneration.

Project description:Macrophages modulate fibrosis during newt lens regeneration.

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Macrophages modulate fibrosis during newt lens regeneration [PWaltl]

Project description:Macrophages modulate fibrosis during newt lens regeneration [PWaltl]

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Macrophages modulate fibrosis during newt lens regeneration [Nvir]

Project description:Macrophages modulate fibrosis during newt lens regeneration [Nvir]

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Chromatin accessibility in response to knockdown of GLI1 and SMARCA2 in GLI1-mediated gene expression.

Project description:GLI1 is a transcription factor correlated to decreased survival in several cancers. We have identified SMARCA2 as a co-regulator that enhances GLI1-mediated transcriptional activity and functions through the C-terminal transcriptional activation domain of GLI1. Central domains including the ATPase motif of SMARCA2 physically interact with GLI1. Evaluation of DNA density indicates GLI1, like SMARCA2, can increase the DNA accessibility with a preference for sites distal to gene transcription start sites and outside the promoter regions (i.e. enhancers). The putative enhancers where accessibility is decreased by the knock down of GLI1 and SMARCA2 are located cis to genes, such as HHIP, that are regulated by GLI1 and implicated in cancer functions. At the putative enhancer for HHIP, the localization of SMARCA2 is at least partially dependent on GLI1’s presence. Understanding this transcriptional regulation by GLI1 and SMARCA2 through altering chromatin accessibility at enhances can provide additional therapeutic targets for cancers dependent on GLI1.

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Gene expression - GLI1 induced mammary gland tumours

Project description:Increased expression of GLI1 is associated with poor prognosis for some breast cancer subtypes. A conditional transgenic GLI1 expressing mouse model, with or without heterozygous deletion of Trp53, was used to generate and study GLI1 induced mammary gland tumours. Tumour tissue was serially orthotopically transplanted for at least 10 generations in NSG mice.

2019-06-30 | E-MTAB-7531 | biostudies-arrayexpress

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