Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction.

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE228472 | GEO | 2023/04/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [scRNA-seq]

Project description:To investigated the functional characteristics and molecular mechanisms underlying senescence in UV irradiated melanocytes. We performed gene expression profiling analysis using data obtained from scRNA-seq of UV-irradiated senescent melanocytes.

2023-04-03 | GSE228471 | GEO

Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [RNA-seq]

2023-04-03 | GSE228470 | GEO

Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction.

Project description:Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction.

| PRJNA949991 | ENA

Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [RNA-seq]

Project description:Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [RNA-seq]

| PRJNA950004 | ENA

Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [scRNA-seq]

Project description:Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [scRNA-seq]

| PRJNA950005 | ENA

Senescent human melanocytes drive skin ageing via paracrine telomere dysfunction.

Project description:Cellular senescence has been shown to contribute to skin ageing. However, the role of melanocytes in the process is understudied. Our data show that melanocytes are the only epidermal cell type to express the senescence marker p16INK4A during human skin ageing. Aged melanocytes also display additional markers of senescence such as reduced HMGB1 and dysfunctional telomeres, without detectable telomere shortening. Additionally, senescent melanocyte SASP induces telomere dysfunction in paracrine manner and limits proliferation of surrounding cells via activation of CXCR3-dependent mitochondrial ROS. Finally, senescent melanocytes impair basal keratinocyte proliferation and contribute to epidermal atrophy in vitro using 3D human epidermal equivalents. Crucially, clearance of senescent melanocytes using the senolytic drug ABT737 or treatment with mitochondria-targeted antioxidant MitoQ suppressed this effect. In conclusion, our study provides proof-of-concept evidence that senescent melanocytes affect keratinocyte function and act as drivers of human skin ageing.

| S-EPMC6885734 | biostudies-literature

Signalling by senescent melanocytes hyperactivates hair growth.

Project description:Niche signals maintain stem cells in a prolonged quiescence or transiently activate them for proper regeneration1. Altering balanced niche signalling can lead to regenerative disorders. Melanocytic skin nevi in human often display excessive hair growth, suggesting hair stem cell hyperactivity. Here, using genetic mouse models of nevi2,3, we show that dermal clusters of senescent melanocytes drive epithelial hair stem cells to exit quiescence and change their transcriptome and composition, potently enhancing hair renewal. Nevus melanocytes activate a distinct secretome, enriched for signalling factors. Osteopontin, the leading nevus signalling factor, is both necessary and sufficient to induce hair growth. Injection of osteopontin or its genetic overexpression is sufficient to induce robust hair growth in mice, whereas germline and conditional deletions of either osteopontin or CD44, its cognate receptor on epithelial hair cells, rescue enhanced hair growth induced by dermal nevus melanocytes. Osteopontin is overexpressed in human hairy nevi, and it stimulates new growth of human hair follicles. Although broad accumulation of senescent cells, such as upon ageing or genotoxic stress, is detrimental for the regenerative capacity of tissue4, we show that signalling by senescent cell clusters can potently enhance the activity of adjacent intact stem cells and stimulate tissue renewal. This finding identifies senescent cells and their secretome as an attractive therapeutic target in regenerative disorders.

| S-EPMC10284692 | biostudies-literature

Targeting senescent dermal fibroblasts responsible for hyperactive melanocytes in melasma.

Project description: Not available

| S-EPMC10325758 | biostudies-literature

Glomerular endothelial derived vesicles mediate podocyte dysfunction via extracellular transfer of miRNA-200c-3p

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

2020-03-05 | GSE129892 | GEO

In vitro evidence for senescent multinucleated melanocytes as a source for tumor-initiating cells.

Project description:Oncogenic signaling in melanocytes results in oncogene-induced senescence (OIS), a stable cell-cycle arrest frequently characterized by a bi- or multinuclear phenotype that is considered as a barrier to cancer progression. However, the long-sustained conviction that senescence is a truly irreversible process has recently been challenged. Still, it is not known whether cells driven into OIS can progress to cancer and thereby pose a potential threat. Here, we show that prolonged expression of the melanoma oncogene N-RAS(61K) in pigment cells overcomes OIS by triggering the emergence of tumor-initiating mononucleated stem-like cells from senescent cells. This progeny is dedifferentiated, highly proliferative, anoikis-resistant and induces fast growing, metastatic tumors. Our data describe that differentiated cells, which are driven into senescence by an oncogene, use this senescence state as trigger for tumor transformation, giving rise to highly aggressive tumor-initiating cells. These observations provide the first experimental in vitro evidence for the evasion of OIS on the cellular level and ensuing transformation.

| S-EPMC4650540 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data