TSG-6 Induces Apoptosis of Human Hypertrophic Scar Fibroblasts via Activation of the Fas/FasL Signalling Pathway
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
30938674
DOI
10.14712/fb2018064050173
PII: file/5882/fb2018a0021.pdf
Knihovny.cz E-resources
- MeSH
- fas Receptor metabolism MeSH
- Apoptosis * MeSH
- Child MeSH
- Adult MeSH
- Fibroblasts pathology MeSH
- Cicatrix, Hypertrophic genetics pathology MeSH
- Humans MeSH
- Fas Ligand Protein metabolism MeSH
- RNA, Messenger genetics metabolism MeSH
- Adolescent MeSH
- Young Adult MeSH
- Cell Adhesion Molecules genetics metabolism MeSH
- Gene Expression Regulation MeSH
- Signal Transduction * MeSH
- Cell Survival MeSH
- Check Tag
- Child MeSH
- Adult MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- fas Receptor MeSH
- FAS protein, human MeSH Browser
- FASLG protein, human MeSH Browser
- Fas Ligand Protein MeSH
- RNA, Messenger MeSH
- Cell Adhesion Molecules MeSH
- TNFAIP6 protein, human MeSH Browser
Tumour necrosis factor-stimulated gene 6 (TSG6) is a protective inflammatory reaction gene which is upregulated by inflammatory processes. Recent studies suggest that TSG-6 exhibits anti-scarring effects. However, the mechanism of TSG-6 action in the scar formation remains poorly understood. We investigated whether TSG-6 affects growth of the human hypertrophic scar fibroblasts (HSFs) via Fas/FasL signalling pathway. Cultured HSFs were transfected with a vector carrying the TSG6 gene (pLVX-Puro-TSG-6) or with a vector not containing the TSG6 gene (pLVX-Puro). Untransfected HSFs served as a control group to both transfected HSFs. The expressions level of TSG-6 was up-regulated in the pLVX-Puro-TSG-6 group at the protein and mRNA level. MTT and flow cytometry were used to assess the effect of TSG-6 on the growth and apoptotic status of HSFs. Finally, qRT-PCR and western blot were used to measure the expression levels of Fas, FasL, FADD, caspase-3 and caspase-8 in each group. The apoptosis rate was significantly enhanced and the growth rate reduced in the HSFs transfected with the TSG6 gene vector. The expression levels of Fas, FasL, FADD, caspase-3 and caspase- 8 were significantly raised in the TSG-6 overexpressing HSFs. It is concluded that increased expression of TSG-6 may induce apoptosis of human hypertrophic scar fibroblasts via activation of the Fas/FasL signalling pathway.
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