Hemopoietic stem cell inhibitor (SCI/MIP-1 alpha) also inhibits clonogenic epidermal keratinocyte proliferation

J Invest Dermatol. 1993 Aug;101(2):113-7. doi: 10.1111/1523-1747.ep12363603.

Abstract

The maintenance and regulation of continuously renewing tissues is ultimately controlled at the level of stem-cell proliferation. We have recently identified a reversible inhibitor of hemopoietic stem-cell proliferation (stem-cell inhibitor [SCI]), which is identical to the macrophage inflammatory protein, MIP-1 alpha, a 69-amino-acid heparin-binding cytokine. To test the cell/tissue specificity of the inhibition of proliferation by SCI/MIP-1 alpha, we have investigated its activity on epidermal keratinocytes, the principal cell type of another continuously renewing tissue. Here we show that SCI/MIP-1 alpha inhibits the proliferation of epidermal keratinocytes in vitro and that the MIP-1 alpha mRNA is present in epidermal Langerhans cells but not in keratinocytes. This suggests an important growth regulatory function for SCI/MIP-1 alpha in keratopoiesis, as well as hemopoiesis, and may also indicate a novel role for the epidermal Langerhans cell. As SCI/MIP-1 alpha can inhibit the proliferation of embryologically distinct precursor cells, this raises the possibility that it may also function in a number of other tissues.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cell Division / drug effects
  • Chemokine CCL4
  • Cytokines / analysis
  • Cytokines / genetics
  • Cytokines / pharmacology*
  • Humans
  • Keratinocytes / cytology*
  • Langerhans Cells / chemistry
  • Macrophage Inflammatory Proteins
  • Mice
  • Monokines / analysis
  • Monokines / genetics
  • Monokines / pharmacology*
  • RNA, Messenger / analysis

Substances

  • Chemokine CCL4
  • Cytokines
  • Macrophage Inflammatory Proteins
  • Monokines
  • RNA, Messenger