Volume 6 Issue 12
Dec.  2015
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Chunji Quan, Moon Kyun Cho, Yuan Shao, Laurel E. Mianecki, Eric Liao, Daniel Perry, Taihao Quan. Dermal fibroblast expression of stromal cellderived factor-1 (SDF-1) promotes epidermal keratinocyte proliferation in normal and diseased skin[J]. Protein&Cell, 2015, 6(12): 890-903. doi: 10.1007/s13238-015-0198-5
Citation: Chunji Quan, Moon Kyun Cho, Yuan Shao, Laurel E. Mianecki, Eric Liao, Daniel Perry, Taihao Quan. Dermal fibroblast expression of stromal cellderived factor-1 (SDF-1) promotes epidermal keratinocyte proliferation in normal and diseased skin[J]. Protein&Cell, 2015, 6(12): 890-903. doi: 10.1007/s13238-015-0198-5

Dermal fibroblast expression of stromal cellderived factor-1 (SDF-1) promotes epidermal keratinocyte proliferation in normal and diseased skin

doi: 10.1007/s13238-015-0198-5
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This work was supported by the National Institute of Health grants ES014697 and ES014697 30S1 (TQ) and Summer Biomedical Research Program (SBRP) University of Michigan Medical School (LM, EL, DP).

  • Received Date: 2015-05-13
  • Rev Recd Date: 2015-07-16
  • 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 realtime 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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