PDGF promotes skin fibrosis via a novel mechanism mediated by signaling through MCHR1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA748403 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15202000_1.fastq.gz | Fastqsanger.gz | |||
| SRR15202000_2.fastq.gz | Fastqsanger.gz | |||
| SRR15202001_1.fastq.gz | Fastqsanger.gz | |||
| SRR15202001_2.fastq.gz | Fastqsanger.gz | |||
| SRR15202002_1.fastq.gz | Fastqsanger.gz |
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Project description:Over expression of PDGF-C in mouse liver resulted in the progression of hepatic fibrosis, steatosis and the development of HCC; this mouse model closely resembles the human HCC that is frequently associated with hepatic fibrosis. Peretinoin (generic name; code, NIK-333), developed by the Kowa Company, (Tokyo, Japan), is an oral acyclic retinoid (ACR) with a vitamin A-like structure that targets the retinoid nuclear receptor. Peretinoin effectively inhibits the progression of hepatic fibrosis and tumors in Pdgf-c Tg mice. Gene expression profiling was evaluated during the progression of hepatic fibrosis and tumors.
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Project description:SOX11 promotes skin fibrosis by inducing fibrotic factors
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Project description:In this study, we demonstrated that baseline SOX11 expression was significantly higher in dermal fibroblasts (DFs) isolated from patients with SSc than that in controls, and increased in response to TGF-b. We then showed that SOX11 is involved in the expression of periostin and some periostin-dependent fibrotic factors identified in lung fibroblasts previously. Moreover, we identified some fibrotic factors induced by SOX11 in DNA microarrays combining TGF-b induction and SOX11 knockdown. Finally, we showed that genetic deletion of SOX11 in Postn positive fibroblast cells protects from bleomycin (BLM)-induced skin fibrosis. Altogether, our data indicate that SOX11 and periostin forms a vicious circle and that TGF-b activates this circle specifically in SSc dermal fibroblasts.
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