Add time:08/07/2019         Source:sciencedirect.com

Human keratinocyte growth factor (KGF) is a recently identified mitogen for epithelial cells produced by normal stromal fibroblasts. KGF has been shown to stimulate keratinocyte migration and promote re-epithelialization of skin suggesting a critical role for KGF in wound healing. To understand how KGF might be regulated during wound healing, we examined the ability of the pro-inflammatory cytokines interleukin-1α (IL-1α), interleukin-1β (IL-1β) interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) transforming growth factor-β1 (TGF-β1) and interferon-γ (IFN-γ) to modulate KGF gene expression in cultured human fibroblasts, using northern blot analysis. Exposure to IL-1α (20 units/ml) or IL-1β (100 units/ml) for 24 h increased KGF mRNA expression by 352% and 504%, respectively, with early induction seen at 2 h and maximal induction seen at 8 h. TNF-α (30 ng/ml) increased KGF mRNA expression by 535% at 24 h, with induction first seen at 8 h. The maximal induction of KGF mRNA was observed when IL-1α, IL-1β and TNF-α were used at 100 units/ml, 100 units/ml and 3 ng/ml, respectively, although concentrations 100–500-fold lower (IL-1α, 0.02 units/ml;IL-β, 0.02 units/ml; and TNF-α, 0.03 ng/ml) were nearly as stimulatory, increasing KGF mRNA expression by 175%, 254% and 322%, respectively. IL-6 (200 units/ml), TGF-β1 (5 ng/ml) and IFN-γ (200 units/ml) did not change the level of KGF mRNA at 24 h in human fibroblasts under the same conditions. The protein synthesis inhibitor cycloheximide abrogated the effects of IL-1α, IL-1β and TNF-α on KGF gene induction, indicating that new protein synthesis is required in the process. Dexamethasone (10−7 M), known to inhibit inflammatory reactions and retard wound healing, also inhibited the induction of KGF mRNA expression by IL-1α, IL-1β and TNF-α. Individual variation in KGF mRNA expression was see when fibroblasts from different aged donors were analysed, but no consistent age-associated change was observed. These results suggest that IL-1α, IL-1β and TNF-α up-regulate KGF gene expression in fibroblasts and might be responsible for its induction following skin wounding or other injury.

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