JUN promotes hypertrophic skin scarring via CD36
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA739661 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14870813_1.fastq.gz | Fastqsanger.gz | |||
| SRR14870813_2.fastq.gz | Fastqsanger.gz | |||
| SRR14870814_1.fastq.gz | Fastqsanger.gz | |||
| SRR14870814_2.fastq.gz | Fastqsanger.gz | |||
| SRR14870815_1.fastq.gz | Fastqsanger.gz |
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Project description:Hypertrophic skin scarring following dermal injury causes extreme pain and psychological trauma for patients. Unfortuately, we do not have effective treatments to prevent or reverse skin scarring. Using RNA and ATAC sequencing of mouse and human fibroblasts, we show that JUN expressing fibroblasts are responsible for skin scarring by regulating CD36 expression. In summary, we show that CD36 antagonism by represent a therapeutic target to overcome JUN hypertrophic skin scarring.
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Project description:We hypothesize that, the mTOR pathway is a dominant pathway in cultured keloid and hypertrophy scar fibriblasts compared to normal skin cells. Certain pathway changes can be detected after medication treatment. Global gene expression in RNA samples from rapamycin and tacrolimus treated fibroblasts (from normal skin and hypertrophic scars, keloid scars) is assayed to study the possibility to use mTOR inhibitors as potential drug to treat abnormal scarring. We investigated the difference between normal wound healing and hypertrophic scars and keloids as well.
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