Abstract
Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic polypeptide hormone known to play an important role as a modulator of hematopoietic processes in human and murine cells. One of the characteristics of TGF-beta 1 is the ability to inhibit the growth of several cell types, including cells of the myeloid lineage. To study the mechanism by which TGF-beta 1 inhibits the growth of myeloid cells, we have used three murine myeloid cell lines, the parental interleukin-3-dependent 32D-123 cell line and two retrovirally infected interleukin-3-independent cell lines (32D-abl, 32D-src), all of which are growth inhibited by TGF-beta 1. Each of these oncogene-transfected cells expresses a greater number of TGF-beta 1 receptors than the parental cell line and responds to TGF-beta 1 with increased sensitivity; 32D and 32D-src cells are 2- and 58-fold more sensitive to TGF-beta 1 inhibition than the parental cell line (ED50 = 35 pM). Both 32D-abl- and 32D-src-transformed cell lines expressed higher levels of the 65- and 85-kDa TGF-beta 1 receptor species than did the parental cells. We observed a correlation between the greater sensitivity of 32D-src cells to TGF-beta 1 and the more rapid down-modulation and reappearance of cell surface TGF-beta 1 receptors on 32D-src cells. Thus, the level of TGF-beta 1 receptor expression and rate of reexpression both have a crucial regulatory effect on the functional activity of the TGF-beta 1 ligand.
Highlights
From the $Laboratoryof Molecular Immunoregulation,Biological Response Modifiers Program, Diuisionof Cancer Treatment, §Biological Carcinogenesis Development Program, ProgramResources, Inc., National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland21702-1201 and the IISterling Research Group, Sterling Drug, Inc., Maluern, Pennsyluania 19355
To induce synthesis of components of the extracellular matrix study the mechanism by whichTGF-81inhibitsthe growth of myeloid cells, we have used three murine myeloid cell lines, the parental interleukin-3-dependent 32D-123 cell line and two retrovirally infected interleukin-3-independentcell lines(32D-abl,32Dsrc), alol f which are growth inhibited TbGyF-81
TGF-/31 plays an importantrole as a differential modulator of the hematopoietic processes (18-22)
Summary
Val. 266, No 15, Issue of May 25, pp. 9617-9621, 1991 Printed in (IS.A. Differential Expression of Transforming GrowthFactor-@1(TGF-@1) Receptors in Murine Myeloid CellLines Transformed with Oncogenes. To induce synthesis of components of the extracellular matrix study the mechanism by whichTGF-81inhibitsthe growth of myeloid cells, we have used three murine myeloid cell lines, the parental interleukin-3-dependent 32D-123 cell line and two retrovirally infected interleukin-3-independentcell lines(32D-abl,32Dsrc), alol f which are growth inhibited TbGyF-81. Each such as fibronectin andcollagen (16, 17). The growth-regulatoryeffects of TGF-(31 vary To study the mechanism of growth inhibition of myeloid depending on cell type. TGF-P1 is known to cells by TGF-Pl, we haveusedaunique system of murine stimulate thegrowth of human and murinemesenchymal cells myeloid cell lines consisting of a parental interleukin-3
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