Keratinocyte-specific modulation of type VII collagen gene expression by pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β)

:  Previous studies have shown that pro‐inflammatory cytokines such as tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β up‐regulate type VII collagen gene (COL7A1) expression in cultured dermal fibroblasts. The present study was designed to investigate the effects of TNF‐α and IL‐1β on COL7A1 e...

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Bibliographic Details
Published in:Experimental dermatology 2005-04, Vol.14 (4), p.289-294
Main Authors: Takeda, Hitoshi, Kon, Atsushi, Ito, Noriko, Sawamura, Daisuke, Takagaki, Keiichi, Hashimoto, Isao, Hanada, Katsumi
Format: Article
Language:English
Subjects:
anchoring fibrils
basement membrane zone
Biological and medical sciences
Blotting, Western
Cell Line, Tumor
Cell Nucleus - metabolism
Cells, Cultured
Collagen Type VII - chemistry
Cytokines - metabolism
Dermatology
epidermal keratinocytes
Gene Expression Regulation
Humans
Inflammation
Interleukin-1 - metabolism
Keratinocytes - metabolism
Medical sciences
RNA, Messenger - metabolism
Signal Transduction
Tumor Necrosis Factor-alpha - metabolism
type VII collagen
Up-Regulation
wound healing
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Summary::  Previous studies have shown that pro‐inflammatory cytokines such as tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β up‐regulate type VII collagen gene (COL7A1) expression in cultured dermal fibroblasts. The present study was designed to investigate the effects of TNF‐α and IL‐1β on COL7A1 expression in epidermal keratinocytes. We demonstrated that both TNF‐α and IL‐1β reduced COL7A1 expression in epidermal keratinocytes in an additive manner, whereas they increased COL7A1 expression in dermal fibroblasts. Thus, regulation of COL7A1 by pro‐inflammatory cytokines is cell type specific. In particular, the inhibitory effects of TNF‐α and IL‐1β occurred, at least in part, at the transcriptional level. Finally, we demonstrated that TNF‐α and IL‐1β enhanced the TGF‐β‐mediated up‐regulation of COL7A1 expression in HaCaT keratinocytes, suggesting that the combination of TGF‐β and TNF‐α or IL‐1β induces a signaling pathway that is completely different from that induced by either pro‐inflammatory cytokine alone.
ISSN:0906-6705
1600-0625
DOI:10.1111/j.0906-6705.2005.00316.x