TY - JOUR
T1 - Growth factor-dependent regulation of transferrin receptor in proliferating and quiescent macrophages
AU - Lokeshwar, Balakrishna L.
AU - Lin, Hsiu San
N1 - Funding Information:
’ This work was supported by U.S. Public Health Service Grants AI-15542 and HL-19746. * Present Address: Department of Urology (D-l), University of Miami, P.O. Box 016217, Miami, FL 33101. 3 To whom correspondencea nd reprint requestss hould be addresseda t Mallinckrodt Institute of Radiology, 5 10 S. Kingshighway, St. Louis, MO 63 1 10.
PY - 1990/10/15
Y1 - 1990/10/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0025000020&partnerID=8YFLogxK
U2 - 10.1016/0008-8749(90)90282-V
DO - 10.1016/0008-8749(90)90282-V
M3 - Article
C2 - 2145079
AN - SCOPUS:0025000020
SN - 0008-8749
VL - 130
SP - 401
EP - 415
JO - Cellular Immunology
JF - Cellular Immunology
IS - 2
ER -