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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE140656 | GEO | 2022/11/16

REPOSITORIES: GEO

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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

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

2022-11-02 | GSE140657 | GEO

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.

2019-09-04 | PXD012353 | Pride

Gene expression profile at single cell level of p16INK4a+ fibroblasts from fibrotic mouse lung

Project description:We studied the role of p16INK4a+ fibroblasts in lung fibrosis. We used single cell RNA seq (scRNA-seq) to characterize p16INK4a+ fibroblasts in fibrotic lung.

2024-04-16 | GSE235352 | GEO

Transcriptional targets of p16INK4A in melanoma

Project description:Expression profiles of 17 melanoma cell lines were analysed to identify genes differentially expressed between cell lines harbouring wild-type or mutant p16INK4A. Relevant paper: Pavey et al. (2007). Note: all of these cell lines contained wild-type p14ARF, so that the transcriptional effects of p16INk4A could be determined without interference from p14ARF. Keywords: Affymetrix Hu133_Plus microarrays

2007-10-01 | GSE7153 | GEO

Allele-specific iChIP-SILAC analysis to identify proteins binding to the p16INK4A gene

Project description:We used insertional ChIP (iChIP) based approach to identify proteins that bind to the p16INK4A gene in the human cell line HCT116. To perform iChIP, we inserted an 8-repeat of the LexA-binding element (LexA-BE) in the p16INK4A promoter region in HCT116. The DNA-binding domain and dimerization domain of the LexA protein fused with the 3xFLAG tag and a nuclear localization signal (NLS) was expressed in the LexA-BE-knock-in cells (#109-2 and #113-5). The resultant cells (#109-2-1 and #113-5-1) were subjected to stable isotope labeling with amino acids in cell culture (SILAC), immunoprecipitated with an anti-FLAG antibody, and subjected to LC-MS/MS analysis.

2024-04-18 | PXD045843 | Pride

Chronic expression of p16INK4a in the epidermis induces Wnt-mediated hyperplasia and promotes tumor initiation (1)

Project description:In this study we examine the outcomes of p16INK4a activation in the adult epidermis. We found that prolonged expression of p16INK4a induces epidermal hyperplasia and dysplasia. We also found that continued p16INK4a expression increased the number of epidermal papillomas that developed after carcinogen treatment. Profling of p16INK4a- expressing cells showed elevated levels of Wnt-pathway ligands and targets, and pharmacologic or genetic Wnt inhibition suppressed p16-induced hyperplasia. In human actinic keratosis, a precursor of squamous cell carcinoma, p16-expressing cells are typically found adjacent to dividing cells, consistent with paracrine interaction. These findings reveal that in addition to its cell-autonomous role in blocking cell proliferation, p16 can induce hyperplasia through paracrine stimulation, suggesting that its activity contributes to the formation of early premalignant epidermal lesions.

2020-04-06 | GSE121728 | GEO

Chronic expression of p16INK4a in the epidermis induces Wnt-mediated hyperplasia and promotes tumor initiation (2)

2020-04-06 | GSE146978 | GEO

Transcription profiling of human melanoma cell lines to identify transcriptional targets of p16INK4A in melanoma

2008-06-15 | E-GEOD-7153 | biostudies-arrayexpress

RNA profiling of p16ink4a-expressing pancreatic beta-cells

Project description:Transcriptome of beta-cells isolated from mice expressing p16ink4a and GFP transgenes and of control β-cells isolated from mice expressing only the GFP transgene

2016-01-20 | GSE76992 | GEO

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