Dermal fibroblast expression of stromal cell-derived factor-1 (SDF-1) promotes epidermal keratinocyte proliferation in normal and diseased skin
- Authors
- Quan, Chunji; Cho, Moon Kyun; Shao, Yuan; Mianecki, Laurel E.; Liao, Eric; Perry, Daniel; Quan, Taihao
- Issue Date
- Dec-2015
- Publisher
- Springer Verlag
- Keywords
- SDF-1; dermal fibroblast; keratinocyte; proliferation; skin cancer; psoriasis
- Citation
- Protein & Cell, v.6, no.12, pp 890 - 903
- Pages
- 14
- Journal Title
- Protein & Cell
- Volume
- 6
- Number
- 12
- Start Page
- 890
- End Page
- 903
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/10097
- DOI
- 10.1007/s13238-015-0198-5
- ISSN
- 1674-800X
1674-8018
- Abstract
- Stromal cells provide a crucial microenvironment for overlying epithelium. Here we investigated the expression and function of a stromal cell-specific protein, stromal cell-derived factor-1 (SDF-1), in normal human skin and in the tissues of diseased skin. Immunohistology and laser capture microdissection (LCM)-coupled quantitative real-time RT-PCR revealed that SDF-1 is constitutively and predominantly expressed in dermal stromal cells in normal human skin in vivo. To our surprise, an extremely high level of SDF-1 transcription was observed in the dermis of normal human skin in vivo, evidenced by much higher mRNA expression level than type I collagen, the most abundant and highly expressed protein in human skin. SDF-1 was also upregulated in the tissues of many human skin disorders including psoriasis, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC). Double immunostaining for SDF-1 and HSP47 (heat shock protein 47), a marker of fibroblasts, revealed that fibroblasts were the major source of stroma-cell-derived SDF-1 in both normal and diseased skin. Functionally, SDF-1 activates the ERK (extracellular-signal-regulated kinases) pathway and functions as a mitogen to stimulate epidermal keratinocyte proliferation. Both overexpression of SDF-1 in dermal fibroblasts and treatment with rhSDF-1 to the skin equivalent cultures significantly increased the number of keratinocyte layers and epidermal thickness. Conversely, the stimulative function of SDF-1 on keratinocyte proliferation was nearly completely eliminated by interfering with CXCR4, a specific receptor of SDF-1, or by knock-down of SDF-1 in fibroblasts. Our data reveal that extremely high levels of SDF-1 provide a crucial microenvironment for epidermal keratinocyte proliferation in both physiologic and pathologic skin conditions.
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- Appears in
Collections - College of Medicine > Department of Dermatology > 1. Journal Articles
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