Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hair follicle stem cell progeny heal blisters while pausing skin development

ABSTRACT: Hair follicle stem cell progeny heal blisters while pausing skin development

PROVIDER: PRJNA647733 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12282480.fastq.gz	Fastqsanger.gz
	SRR12282481.fastq.gz	Fastqsanger.gz
	SRR12282482.fastq.gz	Fastqsanger.gz
	SRR12282483.fastq.gz	Fastqsanger.gz
	SRR12282484.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Hair follicle stem cell progeny heal blisters while pausing skin development

Project description:Injury in adult tissue generally reactivates developmental programs to foster regeneration, but it is not known whether this paradigm applies to growing tissue. Here, by employing blisters, we show that epidermal wounds heal at the expense of skin development. The regenerated epidermis suppresses the expression of tissue morphogenesis genes accompanied by delayed hair follicle (HF) growth. Lineage tracing experiments, cell proliferation dynamics, and mathematical modeling reveal that the progeny of HF junctional zone stem cells, which undergo a morphological transformation, repair the blisters while not promoting HF development. In contrast, the contribution of interfollicular stem cell progeny to blister healing is small. These findings demonstrate that tissue development can be sacrificed for the sake of wound regeneration and suggest that tissue repair does not coincide with the reactivation of developmental programs in all regenerative contexts. Our study elucidates the key cellular mechanism of wound healing in skin blistering diseases.

2021-06-04 | GSE154871 | GEO

Hair follicle stem cell progeny heal blisters while pausing skin development.

Project description:Injury in adult tissue generally reactivates developmental programs to foster regeneration, but it is not known whether this paradigm applies to growing tissue. Here, by employing blisters, we show that epidermal wounds heal at the expense of skin development. The regenerated epidermis suppresses the expression of tissue morphogenesis genes accompanied by delayed hair follicle (HF) growth. Lineage tracing experiments, cell proliferation dynamics, and mathematical modeling reveal that the progeny of HF junctional zone stem cells, which undergo a morphological transformation, repair the blisters while not promoting HF development. In contrast, the contribution of interfollicular stem cell progeny to blister healing is small. These findings demonstrate that HF development can be sacrificed for the sake of epidermal wound regeneration. Our study elucidates the key cellular mechanism of wound healing in skin blistering diseases.

| S-EPMC8256293 | biostudies-literature

Less invasive diagnostics for cancer using hair follicle

Project description:Primary outcome(s): Comparison of the gene expression profile in hair follicle between cancer patients and healthy volunteer

| 2628246 | ecrin-mdr-crc

Dietary restriction delays but cannot heal irradiation-induced hair graying by preserving hair follicle stem cells in quiescence

Project description:DNA damage represents one of the cell intrinsic causes of stem cell aging, which leads to differentiation induced removal of damaged stem cells in skin and blood. Dietary restriction (DR) retards aging across various species including several strains of laboratory mice. Whether, DR has the potential to ameliorate DNA damage driven stem cell exhaustion remains incompletely understood. Here, we show that DR strongly extends the time to hair graying in response to γ–irradiation (IR) induced DNA damage of C57BL/6J mice. The study shows that DR prolongs quiescence of hair follicle stem cells (HFSCs) by silencing gene regulatory networks and metabolic switches that control proliferation and tissue regeneration. DR-mediated prolongation of HSFC quiescence blocks hair growth and prevents the depletion of HFSCs and ckit+ melanoblasts in response to IR. However, prolongation of HSFCs quiescence also leads to a suppression of DNA repair pathways and cannot prevent melanoblast loss and hair graying in the long run, when hair cycling is re- initiated even after extended periods of time. Together, these results support a model indicating that nutrient deprivation can delay but not heal DNA damage driven extinction of HFSCs and melanoblasts by stalling HSFCs in a prolonged state of quiescence coupled with inhibition of DNA repair. Disconnecting these two types of responses to DR could have the potential to delay stem cell aging.

2024-02-21 | GSE156014 | GEO

Dietary restriction delays but cannot heal irradiation-induced hair graying by preserving hair follicle stem cells in quiescence

Project description:Dietary restriction delays but cannot heal irradiation-induced hair graying by preserving hair follicle stem cells in quiescence

| PRJNA656422 | ENA

Gene expression profiling of adult hair follicle dermal stem cells and progeny, dermal sheath and dermal papilla cells

Project description:Here we have developed a novel FACS strategy to prospectively isolate hair follicle dermal stem cells, dermal sheath and dermal papilla cells from adult skin initiating synchronous hair follicle regeneration and identified Hic1 as a marker of hfDSCs and Rspondins as stimulators of hfDSCs and epithelial cells, and subsequently hair follicle regeneration

2020-02-03 | GSE109256 | GEO

Human hair follicle microbiome

Project description:Human hair follicle microbiome

| PRJEB104876 | ENA

Genome-wide maps of histone modifications unwind in vivo chromatin states of the hair follicle lineage [ChIP-Seq]

Project description:Mouse hair follicles undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). During the rest phase, the HF-SCs remain quiescent due to extrinsic inhibitory signals within the niche. As activating cues accumulate, HF-SCs become activated, proliferate, and grows downward to form transient-amplifying matrix progenitor cells. We used ChIP-seq to reveal the genome-wide maps of histone modifications underlying the states of hair follicle stem cells and their transient-amplifying progeny before differentiation. Quiescent hair follicle stem cells (qHF-SCs), activated hair follicle stem cells (aHF-SCs) and transient-amplifying matrix cells (HF-TACs) were FACS-purified for ChIP-sequcencing.

2011-09-02 | E-GEOD-31239 | biostudies-arrayexpress

Genome-wide maps of histone modifications unwind in vivo chromatin states of the hair follicle lineage

Project description:Mouse hair follicles (HFs) undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). During the rest phase, the HF-SCs remain quiescent due to extrinsic inhibitory signals within the niche. As activating cues accumulate, HF-SCs become activated, proliferate, and grow downward to form transient-amplifying matrix progenitor cells. We used microarrays to detect the relative levels of global gene expression underlying the states of hair follicle stem cells and their transient-amplifying progeny before differentiation. Quiescent hair follicle stem cells (qHF-SCs), activated hair follicle stem cells (aHF-SCs) and transient-amplifying matrix cells (HF-TACs) were FACS-purified for RNA extraction and hybridization on Affymetrix microarrays. To obtain homogeneous populations of expression profiles, we applied the FACS technique to purify SC and TACs according to their cell surface markers.

2011-09-01 | E-GEOD-31028 | biostudies-arrayexpress

Autophagy induces hair follicle stem cell activation and hair follicle regeneration by regulating glycolysis

Project description:In this study, in order to explore the role of autophagy of human hair follicle stem cells in hair growth, we explored new ideas for hair regrowth. In this study, rapamycin was used to treat hair follicle stem cells to promote autophagy, and the different expression of genes was observed by comparing with the blank control group.

2024-01-10 | GSE229890 | GEO

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