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Mouse hematopoietic stem-cells and the interaction of c-kit receptor and steel factor

Academic Article
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Overview

authors

  • Ikuta, K.
  • Ingolia, D. E.
  • Friedman, Jeffrey
  • Heimfeld, S.
  • Weissman, I. L.

publication date

  • 1991

journal

  • International Journal of Cell Cloning  Journal

abstract

  • Hematopoietic stem cells (HSCs) are distinguished from other hematopoietic progenitors in bone marrow by their unique ability to undergo multilineage differentiation and self-renewal. Two mouse mutations, dominant spotting (W) and steel (Sl), have pleiotropic effects on hematopoiesis, gametogenesis, and melanoblast development. These two mutations have been shown to be intrinsic (W) and microenvironmental (Sl) defects. Recently, molecular studies revealed that the W and Sl loci encode the c-kit receptor and steel factor (SLF), respectively. The c-kit receptor is expressed on HSCs and hematopoietic progenitors, while SLF is produced by stromal cells. SLF acts on hematopoietic progenitors synergistically with other growth factors. Here we review the effect of these mutations on mouse hematopoiesis, and show that SLF acts on HSCs and other myeloerythroid progenitors, but that it, in our hands, does not play a critical role in HSC generation or self-renewal. Rather, SLF is the most potent co-mitogen (with IL-1, IL-3, IL-6, G-CSF, GM-CSF, or M-CSF) found that acts on these cells, but the effect of such treatments is the rather specific and massive expansion of myeloerythropoiesis, not lymphopoiesis, and perhaps at the expense of HSC self-renewal.

subject areas

  • Animals
  • Hematopoiesis
  • Hematopoietic Cell Growth Factors
  • Hematopoietic Stem Cells
  • Mice
  • Mutation
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-kit
  • Stem Cell Factor
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Research

keywords

  • ANEMIA
  • C-KIT
  • GROWTH FACTOR
  • HEMATOPOIESIS
  • HEMATOPOIETIC STEM CELL
  • PROGENITOR
  • STEEL FACTOR
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Identity

International Standard Serial Number (ISSN)

  • 0737-1454

PubMed ID

  • 1720154
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Additional Document Info

start page

  • 451

end page

  • 460

volume

  • 9

issue

  • 5

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