Activities derived from established human myeloid cell lines reverse the suppression of cell line colony formation by lactoferrin and transferrin

Hal Broxmeyer, B. Y. Rubin, E. Berman, L. Juliano, L. Lu, L. J. Hast, S. Cooper, J. W. Singer

Research output: Contribution to journalArticle

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Abstract

Myeloid cell lines were evaluated for the release of substances needed for colony formation by their own colony-forming cells (CFC) and by other myeloid cell lines. Dialyzed U937 conditioned medium (CM) had no effect on the cloning efficiency of U937 cells, whether or not U937 CFC had been induced for MHC class-II antigens by preincubation of these cells for 72 h with indomethacin and human gamma interferon (HuIFN(γ)). Dialyzed U937 CM, however, restored colony formation of HuIFN(γ)-induced U937 cells suppressed by lactoferrin (LF) or transferrin (TF). Dialyzed U937 CM did not restore colony formation of U937 cells suppressed by acidic isoferritins (AIF) or prostaglandin E2 (PGE2). Detection of the growth-restoring effects of U937 CM required that U937 CM be prepared in the presence of indomethacin or that the CM be dialyzed to remove inhibitors of U937 colony formation. Dialyzed U937 CM did not inactivate LF. Dialyzed U937 CM did not stimulate or enhance colony formation of normal human bone marrow granulocyte-macrophage (CFU-GM), erythroid (BFU-E), or multipotential (CFU-GEMM) progenitor cells, but did contain potent inhibitory activity against these progenitor cells. HL-60, EM2, EM3, and K562 cells were also evaluated. HL-60-, EM3-, and K562-CFC that were not preincubated with HuIFN(γ) did not express MHC class-II antigens, and colony formation by these cells was not influenced by LF, TF, or AIF. Noninduced EM2-CFC constitutively expressed MHC class-II antigens, and colony formation by these cells was suppressed by LF, TF, and AIF. After induction of MHC class-II antigens on HL-60- and EM3-CFC by HuIFN(γ), colony formation by these cells was suppressed by LF, TF, and AIF. Colony formation by HuIFN(γ)-induced EM2 cells was more responsive to inhibition by LF, TF, and AIF than was colony formation by noninduced EM2 cells. K562 cells were not induced into a responsive state to LF, TF, or AIF by HuIFN(γ). Dialyzed CM from HL-60, EM2, and EM3 cells contained activities that restored colony formation by their own LF-suppressed CFC. The activities present in dialyzed CM from U937, HL-60, EM2, and EM3 cells may be similar since they could each restore LF-suppressed colony formation of U937, HL-60, EM2, or EM3 cells. The dialyzed CM from HL-60, EM2, and EM3 cells had to be pretreated with anti-acidic isoferritin antiserum in order to demonstrate a growth-restoring effect on U937 cells since these cells were more sensitive than the other cell lines to the acidic isoferritin-inhibiting activity present in the dialyzed CM from HL-60, EM2, and EM3 cells. The myeloid cell lines, U937, HL-60, EM2, and EM3 can thus serve as models for studies on the stimulatory and inhibitory regulation of myeloid cell line proliferation.

Original languageEnglish
Pages (from-to)51-59
Number of pages9
JournalExperimental Hematology
Volume14
Issue number1
StatePublished - 1986

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Lactoferrin
Myeloid Cells
Transferrin
Conditioned Culture Medium
Cell Line
U937 Cells
Histocompatibility Antigens Class II
K562 Cells
Indomethacin
Stem Cells
Myeloid Progenitor Cells
Granulocyte-Macrophage Progenitor Cells
Erythroid Precursor Cells
acidic isoferritin

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Genetics
  • Hematology
  • Oncology
  • Transplantation

Cite this

Activities derived from established human myeloid cell lines reverse the suppression of cell line colony formation by lactoferrin and transferrin. / Broxmeyer, Hal; Rubin, B. Y.; Berman, E.; Juliano, L.; Lu, L.; Hast, L. J.; Cooper, S.; Singer, J. W.

In: Experimental Hematology, Vol. 14, No. 1, 1986, p. 51-59.

Research output: Contribution to journalArticle

Broxmeyer, Hal ; Rubin, B. Y. ; Berman, E. ; Juliano, L. ; Lu, L. ; Hast, L. J. ; Cooper, S. ; Singer, J. W. / Activities derived from established human myeloid cell lines reverse the suppression of cell line colony formation by lactoferrin and transferrin. In: Experimental Hematology. 1986 ; Vol. 14, No. 1. pp. 51-59.
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abstract = "Myeloid cell lines were evaluated for the release of substances needed for colony formation by their own colony-forming cells (CFC) and by other myeloid cell lines. Dialyzed U937 conditioned medium (CM) had no effect on the cloning efficiency of U937 cells, whether or not U937 CFC had been induced for MHC class-II antigens by preincubation of these cells for 72 h with indomethacin and human gamma interferon (HuIFN(γ)). Dialyzed U937 CM, however, restored colony formation of HuIFN(γ)-induced U937 cells suppressed by lactoferrin (LF) or transferrin (TF). Dialyzed U937 CM did not restore colony formation of U937 cells suppressed by acidic isoferritins (AIF) or prostaglandin E2 (PGE2). Detection of the growth-restoring effects of U937 CM required that U937 CM be prepared in the presence of indomethacin or that the CM be dialyzed to remove inhibitors of U937 colony formation. Dialyzed U937 CM did not inactivate LF. Dialyzed U937 CM did not stimulate or enhance colony formation of normal human bone marrow granulocyte-macrophage (CFU-GM), erythroid (BFU-E), or multipotential (CFU-GEMM) progenitor cells, but did contain potent inhibitory activity against these progenitor cells. HL-60, EM2, EM3, and K562 cells were also evaluated. HL-60-, EM3-, and K562-CFC that were not preincubated with HuIFN(γ) did not express MHC class-II antigens, and colony formation by these cells was not influenced by LF, TF, or AIF. Noninduced EM2-CFC constitutively expressed MHC class-II antigens, and colony formation by these cells was suppressed by LF, TF, and AIF. After induction of MHC class-II antigens on HL-60- and EM3-CFC by HuIFN(γ), colony formation by these cells was suppressed by LF, TF, and AIF. Colony formation by HuIFN(γ)-induced EM2 cells was more responsive to inhibition by LF, TF, and AIF than was colony formation by noninduced EM2 cells. K562 cells were not induced into a responsive state to LF, TF, or AIF by HuIFN(γ). Dialyzed CM from HL-60, EM2, and EM3 cells contained activities that restored colony formation by their own LF-suppressed CFC. The activities present in dialyzed CM from U937, HL-60, EM2, and EM3 cells may be similar since they could each restore LF-suppressed colony formation of U937, HL-60, EM2, or EM3 cells. The dialyzed CM from HL-60, EM2, and EM3 cells had to be pretreated with anti-acidic isoferritin antiserum in order to demonstrate a growth-restoring effect on U937 cells since these cells were more sensitive than the other cell lines to the acidic isoferritin-inhibiting activity present in the dialyzed CM from HL-60, EM2, and EM3 cells. The myeloid cell lines, U937, HL-60, EM2, and EM3 can thus serve as models for studies on the stimulatory and inhibitory regulation of myeloid cell line proliferation.",
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TY - JOUR

T1 - Activities derived from established human myeloid cell lines reverse the suppression of cell line colony formation by lactoferrin and transferrin

AU - Broxmeyer, Hal

AU - Rubin, B. Y.

AU - Berman, E.

AU - Juliano, L.

AU - Lu, L.

AU - Hast, L. J.

AU - Cooper, S.

AU - Singer, J. W.

PY - 1986

Y1 - 1986

N2 - Myeloid cell lines were evaluated for the release of substances needed for colony formation by their own colony-forming cells (CFC) and by other myeloid cell lines. Dialyzed U937 conditioned medium (CM) had no effect on the cloning efficiency of U937 cells, whether or not U937 CFC had been induced for MHC class-II antigens by preincubation of these cells for 72 h with indomethacin and human gamma interferon (HuIFN(γ)). Dialyzed U937 CM, however, restored colony formation of HuIFN(γ)-induced U937 cells suppressed by lactoferrin (LF) or transferrin (TF). Dialyzed U937 CM did not restore colony formation of U937 cells suppressed by acidic isoferritins (AIF) or prostaglandin E2 (PGE2). Detection of the growth-restoring effects of U937 CM required that U937 CM be prepared in the presence of indomethacin or that the CM be dialyzed to remove inhibitors of U937 colony formation. Dialyzed U937 CM did not inactivate LF. Dialyzed U937 CM did not stimulate or enhance colony formation of normal human bone marrow granulocyte-macrophage (CFU-GM), erythroid (BFU-E), or multipotential (CFU-GEMM) progenitor cells, but did contain potent inhibitory activity against these progenitor cells. HL-60, EM2, EM3, and K562 cells were also evaluated. HL-60-, EM3-, and K562-CFC that were not preincubated with HuIFN(γ) did not express MHC class-II antigens, and colony formation by these cells was not influenced by LF, TF, or AIF. Noninduced EM2-CFC constitutively expressed MHC class-II antigens, and colony formation by these cells was suppressed by LF, TF, and AIF. After induction of MHC class-II antigens on HL-60- and EM3-CFC by HuIFN(γ), colony formation by these cells was suppressed by LF, TF, and AIF. Colony formation by HuIFN(γ)-induced EM2 cells was more responsive to inhibition by LF, TF, and AIF than was colony formation by noninduced EM2 cells. K562 cells were not induced into a responsive state to LF, TF, or AIF by HuIFN(γ). Dialyzed CM from HL-60, EM2, and EM3 cells contained activities that restored colony formation by their own LF-suppressed CFC. The activities present in dialyzed CM from U937, HL-60, EM2, and EM3 cells may be similar since they could each restore LF-suppressed colony formation of U937, HL-60, EM2, or EM3 cells. The dialyzed CM from HL-60, EM2, and EM3 cells had to be pretreated with anti-acidic isoferritin antiserum in order to demonstrate a growth-restoring effect on U937 cells since these cells were more sensitive than the other cell lines to the acidic isoferritin-inhibiting activity present in the dialyzed CM from HL-60, EM2, and EM3 cells. The myeloid cell lines, U937, HL-60, EM2, and EM3 can thus serve as models for studies on the stimulatory and inhibitory regulation of myeloid cell line proliferation.

AB - Myeloid cell lines were evaluated for the release of substances needed for colony formation by their own colony-forming cells (CFC) and by other myeloid cell lines. Dialyzed U937 conditioned medium (CM) had no effect on the cloning efficiency of U937 cells, whether or not U937 CFC had been induced for MHC class-II antigens by preincubation of these cells for 72 h with indomethacin and human gamma interferon (HuIFN(γ)). Dialyzed U937 CM, however, restored colony formation of HuIFN(γ)-induced U937 cells suppressed by lactoferrin (LF) or transferrin (TF). Dialyzed U937 CM did not restore colony formation of U937 cells suppressed by acidic isoferritins (AIF) or prostaglandin E2 (PGE2). Detection of the growth-restoring effects of U937 CM required that U937 CM be prepared in the presence of indomethacin or that the CM be dialyzed to remove inhibitors of U937 colony formation. Dialyzed U937 CM did not inactivate LF. Dialyzed U937 CM did not stimulate or enhance colony formation of normal human bone marrow granulocyte-macrophage (CFU-GM), erythroid (BFU-E), or multipotential (CFU-GEMM) progenitor cells, but did contain potent inhibitory activity against these progenitor cells. HL-60, EM2, EM3, and K562 cells were also evaluated. HL-60-, EM3-, and K562-CFC that were not preincubated with HuIFN(γ) did not express MHC class-II antigens, and colony formation by these cells was not influenced by LF, TF, or AIF. Noninduced EM2-CFC constitutively expressed MHC class-II antigens, and colony formation by these cells was suppressed by LF, TF, and AIF. After induction of MHC class-II antigens on HL-60- and EM3-CFC by HuIFN(γ), colony formation by these cells was suppressed by LF, TF, and AIF. Colony formation by HuIFN(γ)-induced EM2 cells was more responsive to inhibition by LF, TF, and AIF than was colony formation by noninduced EM2 cells. K562 cells were not induced into a responsive state to LF, TF, or AIF by HuIFN(γ). Dialyzed CM from HL-60, EM2, and EM3 cells contained activities that restored colony formation by their own LF-suppressed CFC. The activities present in dialyzed CM from U937, HL-60, EM2, and EM3 cells may be similar since they could each restore LF-suppressed colony formation of U937, HL-60, EM2, or EM3 cells. The dialyzed CM from HL-60, EM2, and EM3 cells had to be pretreated with anti-acidic isoferritin antiserum in order to demonstrate a growth-restoring effect on U937 cells since these cells were more sensitive than the other cell lines to the acidic isoferritin-inhibiting activity present in the dialyzed CM from HL-60, EM2, and EM3 cells. The myeloid cell lines, U937, HL-60, EM2, and EM3 can thus serve as models for studies on the stimulatory and inhibitory regulation of myeloid cell line proliferation.

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