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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.

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Gli1<sup>+</sup> mesenchymal stromal cells form a pathological niche to promote airway progenitor metaplasia in the fibrotic lung.

Project description:Aberrant epithelial reprogramming can induce metaplastic differentiation at sites of tissue injury that culminates in transformed barriers composed of scar and metaplastic epithelium. While the plasticity of epithelial stem cells is well characterized, the identity and role of the niche has not been delineated in metaplasia. Here, we show that Gli1+ mesenchymal stromal cells (MSCs), previously shown to contribute to myofibroblasts during scarring, promote metaplastic differentiation of airway progenitors into KRT5+ basal cells. During fibrotic repair, Gli1+ MSCs integrate hedgehog activation signalling to upregulate BMP antagonism in the progenitor niche that promotes metaplasia. Restoring the balance towards BMP activation attenuated metaplastic KRT5+ differentiation while promoting adaptive alveolar differentiation into SFTPC+ epithelium. Finally, fibrotic human lungs demonstrate altered BMP activation in the metaplastic epithelium. These findings show that Gli1+ MSCs integrate hedgehog signalling as a rheostat to control BMP activation in the progenitor niche to determine regenerative outcome in fibrosis.

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Nuclear receptors Nur77 and Nurr1 modulate mesenchymal stromal cell migration

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