Fol. Biol. 2018, 64, 173-181

https://doi.org/10.14712/fb2018064050173

TSG-6 Induces Apoptosis of Human Hypertrophic Scar Fibroblasts via Activation of the Fas/FasL Signalling Pathway

X.-Y. Li, T. Li, Xiao-Jing Li, J.-N. Wang, Z. Chen

Department of Plastic Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, China

Received September 2018
Accepted November 2018

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.

Funding

The authors wish to thank the Science and Technique Foundation of Anhui Province of China (1604a0802078).

References

29 live references