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Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung [scRNA-Seq]

ABSTRACT: Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung [scRNA-Seq]

PROVIDER: PRJNA590469 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10493723.fastq.gz	Fastqsanger.gz
	SRR10493724.fastq.gz	Fastqsanger.gz

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Similar Datasets

Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung

Project description:Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung

| PRJNA590466 | ENA

Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung [RNA-Seq]

Project description:Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung [RNA-Seq]

| PRJNA590468 | ENA

Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung [RNA-Seq]

Project description:We collected freshly sorted mesenchyme (live CD45-Epcam-CD31-PDGFRa+GFP- or GFP+) from dissociated lung tissue of INKBRITE animals to characterize the transcriptome difference between p16INK4a+ vs p16INK4a- cells at homeostasis and during injury. We used fluorescence activated cell sorting (FACS) to exclude immune (CD45+), epithelial (Epcam+), and endothelial (CD31+) cells and positively select for PDGFRa+ mesenchyme. Cells were sequenced at a depth of average of 45 million reads/sample. The results revealed an increase of senescence associated secretory phenotype (SASP) signature in p16INK4+ cells that becomes refined after injury. We found the expression of an epithelial growth factor epiregulin (ereg) increased in p16INK4a+ cells after injury suggesting a possible role of p16INK4a+ senescence during regeneration of lung epithelium.

2022-11-02 | GSE140654 | GEO

Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung [scRNA-Seq]

Project description:A single-cell transcriptional analysis was performed on p16INK4a+ cells from the adult murine lung. Whole adult murine lung tissue was dissociated to single cells and subjected to fluorescence activated cell sorting (FACS) to select all live p16INK4a + cells. The single cell RNA-sequencing library was then subsequently generated. Cells were sequenced at a depth of ~30,506 mean reads/cell. We captured approximately 8752 cells with a mean of 2457 genes detected per cell utilizing a droplet-based barcoding approach to capture single cells for RNA sequencing. The results demonstrate that the p16INK4a + population are predominantly in the immune CD45+ populations and PDGFRa+ mesenchyme.

2022-11-16 | GSE140656 | GEO

Sentinel p16INK4a+ cells in the basement membrane form a reparative niche in the lung

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

2022-11-02 | GSE140657 | GEO

Sentinel <i>p16</i><sup>INK4a+</sup> cells in the basement membrane form a reparative niche in the lung.

Project description:We engineered an ultrasensitive reporter of p16INK4a, a biomarker of cellular senescence. Our reporter detected p16INK4a-expressing fibroblasts with certain senescent characteristics that appeared shortly after birth in the basement membrane adjacent to epithelial stem cells in the lung. Furthermore, these p16INK4a+ fibroblasts had enhanced capacity to sense tissue inflammation and respond through their increased secretory capacity to promote epithelial regeneration. In addition, p16INK4a expression was required in fibroblasts to enhance epithelial regeneration. This study highlights a role for p16INK4a+ fibroblasts as tissue-resident sentinels in the stem cell niche that monitor barrier integrity and rapidly respond to inflammation to promote tissue regeneration.

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Sentinel REACT

Project description:Sentinel REACT

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Sentinel REACT

Project description:Sentinel REACT

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Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16INK4A

Project description:p16INK4A inhibits the CDK4/6 kinases and is therefore an important cell cycle regulator. Accumulation of p16INK4A in response to oncogenic transformation leads to cellular senescence and it is therefore frequently lost in cancer. p16INK4A is also known to accumulate under conditions of cellular oxidative stress and therefore could potentially be regulated by redox signaling, which is a form of signal transduction that is mediated by the reversible oxidation of cysteine-thiol side chains in proteins. We found that oxidation of the single cysteine residue in p16INK4A in human cells occurs under relatively mild oxidizing conditions and that this leads to disulfide dependent dimerization. p16INK4A is a well-characterized all alpha-helical protein, but we find that upon cysteine-dependent dimerization, p16INK4A undergoes a dramatic structural rearrangement and forms aggregates that have the typical features of amyloid fibrils, including binding of diagnostic dyes, presence of cross-β sheet structure, and typical dimensions found in electron microscopy. We find that p16INK4A amyloid formation abolishes its function as a CDK4/6 inhibitor in human cells. Taken together, these observations mechanistically link the cellular redox state to the inactivation of p16INK4A through the formation of amyloid fibrils.

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Topical lubrication restores dry eye corneal stroma by producing reparative keratocytesacripep promotes corneal regeneration in autoimmune mediated dry eye disease (snRNA-Seq).

Project description:Topical lubrication is the most common remedy for relieving the signs and symptoms of dry eye. However, the therapeutic value of lubricating the ocular surface remains relatively unknown. Here we reveal the restorative properties of the simplest form of lubrication in a mouse model of autoimmune-mediated dry eye. We show topical treatment with PBS rescues corneal stromal architecture through restoring the basement membrane and collagen fiber alignment essential for maintaining corneal transparency. At the single cell level we show keratocytes exhibit significant plasticity under chronic injury, with continuous transition from a homeostatic to inflammatory state, and that lubrication converts these inflammatory cells to a unique reparative phenotype. We further identify IL1b-IL1R1-MAPK signaling as a key pathway driving keratocyte inflammation, and that disruption of the IL1b autocrine amplification loop by lubrication is sufficient to reprogram the inflammatory keratocytes towards the reparative state. Thus, our study underscores the regenerative potential of topical lubrication in dry eye, and reveals fibroblast-targeted therapies as a novel approach to restoring ocular surface health.

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