Involvement of insulin-like growth factor-I in psoriasis as a paracrine growth factor: dermal fibroblasts play a regulatory role in developing psoriatic lesions

H Miura, S Sano, M Higashiyama, K Yoshikawa… - Archives of …, 2000 - Springer
H Miura, S Sano, M Higashiyama, K Yoshikawa, S Itami
Archives of dermatological research, 2000Springer
To investigate the contribution of dermal fibroblasts to the development of psoriasis, we
examined the expression of mRNA for insulin-like growth factor-I (IGF-I) and its regulator IGF-
I binding proteins (IGFBPs) in psoriatic fibroblasts by RT-PCR. We also studied the effect of
inflammatory cytokines including interferon gamma (IFN-γ), tumor necrosis factor alfa (TNF-
α), and IFN-α on the expression of IGF-I and IGFBPs in the fibroblasts. Semiquantitative
analysis revealed that IGF-I mRNA expression in psoriatic fibroblasts (PF) was significantly …
Abstract To investigate the contribution of dermal fibroblasts to the development of psoriasis, we examined the expression of mRNA for insulin-like growth factor-I (IGF-I) and its regulator IGF-I binding proteins (IGFBPs) in psoriatic fibroblasts by RT-PCR. We also studied the effect of inflammatory cytokines including interferon gamma (IFN-γ), tumor necrosis factor alfa (TNF-α), and IFN-α on the expression of IGF-I and IGFBPs in the fibroblasts. Semiquantitative analysis revealed that IGF-I mRNA expression in psoriatic fibroblasts (PF) was significantly higher than in control fibroblasts (CF). However, no significant difference in IGF-I mRNA was shown between nonlesional psoriatic fibroblasts (NF) and CF. Treatment with IFN-α in vitro upregulated IGF-I mRNA in PF and in CF. TNF-α appeared to downregulate IGF-I mRNA in PF but had no effect on CF. IFN-γ did not show a significant effect on IGF-I mRNA levels in any type of fibroblast. IGFBP-3 mRNA was expressed equally in PF and CF, and was not affected by cytokines. The expression of IGFBP-5 mRNA in PF was downregulated by IFN-γ and TNF-α. Taken together, these results indicate that dermal fibroblasts may contribute to the epidermal hyperplasia of psoriasis by promoting keratinocyte proliferation through IGF-I, whose secretion could be modulated by inflammatory cytokines.
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