Abstract
Transferrin receptor (TfR) expression in a population of murine macrophages was investigated during the colony-stimulating factor-1 (CSF-1)-induced proliferation and quiescence. Depletion of CSF-1 from the culture medium of bone marrow cell-derived macrophages (BMM) resulted in a simultaneous decrease in the total (cell surface + intracellular) amount of TfR and complete cessation of proliferating activity ([3H]thymidine incorporation). The addition of CSF-1 to quiescent BMM resulted in a bimodal increase in surface TfR activity. A rapid but transient twofold increase only on the cell surface due to changes in the cycling of TfR was followed by a steady increase of total cellular TfR due to de novo synthesis. A similar transient increase in surface TfR was also induced by another hemopoietic colony-stimulating factor, GM-CSF, which is mitogenic for BMM. IL-3, which did not stimulate the clonal growth of these cells, failed to modulate surface TfR. In contrast to its effect on the cycling rate of TfR in quiescent cells, CSF-1 had little effect on the TfR distribution on proliferating BMM as well as on the J774 cells (a macrophage-like tumor cell line) despite the latter expressing high levels of CSF-1 receptor. This study showed that (i) cell surface modulation by growth factor is a function of state of cellular proliferation, and (ii) rapid changes in the cell surface distribution of TfR result from changes in its cycling rates.
Original language | English (US) |
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Pages (from-to) | 401-415 |
Number of pages | 15 |
Journal | Cellular Immunology |
Volume | 130 |
Issue number | 2 |
DOIs | |
State | Published - Oct 15 1990 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology