Abstract
CSF-1 is a hematopoietic growth factor that specifically causes the proliferation and differentiation of mononuclear phagocytic cells. J774 cells are a monocyte precursor-like macrophage cell line. This transformed macrophage cell line exhibits specific 125I-CSF-1-binding activity similar to that of normal murine macrophages, although its survival and growth is independent of CSF-1. At 0°C, saturation of binding sites was achieved at 250 pM 125I-CSF-1. At 37° C, the bound 125I-CSF-1 was rapidly internalized and degraded by the target cells with a T( 1/2 ) of approximately 30 min; degradation was inhibited by the addition of NH4Cl. The addition of CSF-1 to cultures caused dose-dependent inhibition rather than stimulation of [3H]thymidine uptake by J774 cells. Whereas CSF-1 stimulated the clonal growth of normal mouse peritoneal exudate macrophages, it inhibited the clonal growth of J774 cells in agar cultures. Furthermore, CSF-1 exhibited a concentration-dependent enhancement of the production of plasminogen activator (PA) by J774 cells. The enhanced production of PA was detected 6 hr after the addition of CSF-1 and was inhibited by the simultaneous addition of the anti-inflammatory drug. It appears that the effects of CSF-1 on cell proliferation and PA production by CSF-1 receptor-bearing cells are mediated by distinct intracellular pathways albeit through the same receptor.
Original language | English |
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Pages (from-to) | 2955-2960 |
Number of pages | 6 |
Journal | Journal of Immunology |
Volume | 132 |
Issue number | 6 |
State | Published - 1984 |