Upregulation of Collagen Generation by IL-13 in Human Keloid Fibroblasts Strain via the STAT6 Signaling Pathways

Abstract: Hypertrophic scar and keloids are frequent and severe form of fibrosis of the skin， scar tissue is the product of repairing human body after injury. Interleukin (IL)-13 has been implicated in the pathogenesis of various diseases characterized by fibrosis. In this study we observed the effects of recombinant interleukin-13(rIL- 13) on collagen generation from keloid fibroblasts strain(CRL-1762) and explored its mechanism. CRL-1762 cells were divided into two groups: the treated group was treated with rIL-13(100 μg/L) and the control was without rIL- 13 treatment. The effects of rIL-13 on the growth of CRL-1762 cells were detected by cell counting experiment and HE staining. The Hydroxyproline(Hyp) release assay was used to measure total collagen content of the culture supernatant. The expression of IL-13 receptor α1 was determined by RT-PCR. Western blot was used to analyze the level of STAT6 phosphorylated. The results showed that rIL-13 induced significant proliferation of cells and significantly increased Hyp secretion (P<0.01). The expression of IL-13 receptor α1mRNA was detected in CRL- 1762 cells. The level of phosphorylated STAT6 protein in 2h was significantly higher than that in other time， the level of phosphorylated STAT6 has been decreased after 4h of stimulation with IL-13. These demonstrated that IL-13 receptor á1 expression in human keloid fibroblast was observed and rIL-13 upregulated the collagen generation via the STAT6 signaling pathways.

CSTR: 32200.14.cjcb.2010.06.0006