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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE140657 | GEO | 2022/11/02

REPOSITORIES: GEO

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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 [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 <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 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

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

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

| PRJNA590469 | 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]

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Specific 3-O-sulfated heparan sulfate domains regulate salivary gland basement membrane metabolism and epithelial differentiation

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

2024-08-01 | GSE235187 | GEO

The basement membrane of hair follicle stem cells is a muscle cell niche.

Project description:The hair follicle bulge in the epidermis associates with the arrector pili muscle (APM) that is responsible for piloerection ("goosebumps"). We show that stem cells in the bulge deposit nephronectin into the underlying basement membrane, thus regulating the adhesion of mesenchymal cells expressing the nephronectin receptor, ?8?1 integrin, to the bulge. Nephronectin induces ?8 integrin-positive mesenchymal cells to upregulate smooth muscle markers. In nephronectin knockout mice, fewer arrector pili muscles form in the skin, and they attach to the follicle above the bulge, where there is compensatory upregulation of the nephronectin family member EGFL6. Deletion of ?8 integrin also abolishes selective APM anchorage to the bulge. Nephronectin is a Wnt target; epidermal ?-catenin activation upregulates epidermal nephronectin and dermal ?8 integrin expression. Thus, bulge stem cells, via nephronectin expression, create a smooth muscle cell niche and act as tendon cells for the APM. Our results reveal a functional role for basement membrane heterogeneity in tissue patterning. PAPERCLIP:

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Project description: Not available

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Basement membrane and stroke.

Project description:Located at the interface of the circulation system and the CNS, the basement membrane (BM) is well positioned to regulate blood-brain barrier (BBB) integrity. Given the important roles of BBB in the development and progression of various neurological disorders, the BM has been hypothesized to contribute to the pathogenesis of these diseases. After stroke, a cerebrovascular disease caused by rupture (hemorrhagic) or occlusion (ischemic) of cerebral blood vessels, the BM undergoes constant remodeling to modulate disease progression. Although an association between BM dissolution and stroke is observed, how each individual BM component changes after stroke and how these components contribute to stroke pathogenesis are mostly unclear. In this review, I first briefly introduce the composition of the BM in the brain. Next, the functions of the BM and its major components in BBB maintenance under homeostatic conditions are summarized. Furthermore, the roles of the BM and its major components in the pathogenesis of hemorrhagic and ischemic stroke are discussed. Last, unsolved questions and potential future directions are described. This review aims to provide a comprehensive reference for future studies, stimulate the formation of new ideas, and promote the generation of new genetic tools in the field of BM/stroke research.

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