Genetic analysis of denritic cell and macrophage differentiation from myb-transformed myeloid cell lines

To gain some insight into the role of c-fes in macrophage differentiation, we have analyzed the ability of HL60 leukemic promyelocytic cells and FDC-P1/MAC-11 murine myeloid precursor cells to differentiate in response to phorbol esters after inhibition of c-fes function. Fes inactivation has been obtained by using oligodeoxynucleotides (ODN) complementary to the 5′ region of c-fes mRNA and to 5′ splice junctions of c-fes primary transcript. After 5 days (d) in culture, in several separate experiments performed with different ODN preparations, a complete inhibition of c-fes expression was observed in HL60 and in FDC-P1/MAC-11 cells. No perturbation of cell growth was evident in our experimental conditions in both cell lines after c-fes inhibition. Furthermore, in HL60 cells lacking c-fes product, an almost complete downregulation of the α4β1 fibronectin receptor occurred. However, in both cell lines, the induction of macrophage differentiation by phorbol esters resulted in an almost complete maturation arrest as evaluated by morphological, cytochemical, immunological criteria, and by the cytofluorimetric cell cycle analysis. A loss of the adhesion capacity of both myeloid cell lines, when compared to terminally differentated macrophages, was also observed. These results suggest that HL60 and FDC-P1/MAC-11 cells, when treated with phorbol 12-myristate 13-acetate, require c-fes protein expression to activate the genetic program underlying macrophage differentiation.

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Antisense Inhibition of c-fes Proto-oncogene Blocks PMA-Induced Macrophage Differentiation in HL60 and in FDC-P1/MAC-11 Cells

Blood ◽

10.1182/blood.v89.1.135 ◽

1997 ◽

Vol 89 (1) ◽

pp. 135-145 ◽

Cited By ~ 26

Author(s):

Rossella Manfredini ◽

Raffaella Balestri ◽

Enrico Tagliafico ◽

Francesca Trevisan ◽

Michela Pizzanelli ◽

...

Keyword(s):

Cell Lines ◽

Phorbol Esters ◽

Myeloid Cell ◽

Macrophage Differentiation ◽

Primary Transcript ◽

Experimental Conditions ◽

Fibronectin Receptor ◽

Splice Junctions ◽

Insight Into

Abstract To gain some insight into the role of c-fes in macrophage differentiation, we have analyzed the ability of HL60 leukemic promyelocytic cells and FDC-P1/MAC-11 murine myeloid precursor cells to differentiate in response to phorbol esters after inhibition of c-fes function. Fes inactivation has been obtained by using oligodeoxynucleotides (ODN) complementary to the 5′ region of c-fes mRNA and to 5′ splice junctions of c-fes primary transcript. After 5 days (d) in culture, in several separate experiments performed with different ODN preparations, a complete inhibition of c-fes expression was observed in HL60 and in FDC-P1/MAC-11 cells. No perturbation of cell growth was evident in our experimental conditions in both cell lines after c-fes inhibition. Furthermore, in HL60 cells lacking c-fes product, an almost complete downregulation of the α4β1 fibronectin receptor occurred. However, in both cell lines, the induction of macrophage differentiation by phorbol esters resulted in an almost complete maturation arrest as evaluated by morphological, cytochemical, immunological criteria, and by the cytofluorimetric cell cycle analysis. A loss of the adhesion capacity of both myeloid cell lines, when compared to terminally differentated macrophages, was also observed. These results suggest that HL60 and FDC-P1/MAC-11 cells, when treated with phorbol 12-myristate 13-acetate, require c-fes protein expression to activate the genetic program underlying macrophage differentiation.

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Reversible macrophage differentiation induced in a new human myeloid cell line by gamma interferon.

Cell Biology International ◽

10.1006/cbir.1995.1002 ◽

1995 ◽

Vol 19 (1) ◽

pp. 9-16

Author(s):

C Pintér

Keyword(s):

Cell Line ◽

Myeloid Cell ◽

Gamma Interferon ◽

Macrophage Differentiation ◽

Myeloid Cell Line

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Nanoparticles for Directed Immunomodulation: Mannose-Functionalized Glycodendrimers Induce Interleukin-8 in Myeloid Cell Lines

Biomacromolecules ◽

10.1021/acs.biomac.1c00476 ◽

2021 ◽

Author(s):

Izabela Jatczak-Pawlik ◽

Michał Gorzkiewicz ◽

Maciej Studzian ◽

Robin Zinke ◽

Dietmar Appelhans ◽

...

Keyword(s):

Cell Lines ◽

Myeloid Cell ◽

Interleukin 8

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The c-myc oncogene is regulated independently of differentiation in myeloid cell lines

Leukemia Research ◽

10.1016/0145-2126(89)90053-2 ◽

1989 ◽

Vol 13 (8) ◽

pp. 651-659 ◽

Cited By ~ 10

Author(s):

Pamela Roberts ◽

Mark Jones ◽

Rosemary Gale ◽

Shaun Thomas ◽

Nicholas Tidman ◽

...

Keyword(s):

Cell Lines ◽

Myeloid Cell ◽

Myc Oncogene

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Cell membrane-associated proteoglycans mediate extramedullar myeloid proliferation in granulomatous inflammatory reactions to schistosome eggs

Journal of Cell Science ◽

10.1242/jcs.104.2.477 ◽

1993 ◽

Vol 104 (2) ◽

pp. 477-484

Author(s):

M. Alvarez-Silva ◽

L.C. da Silva ◽

R. Borojevic

Keyword(s):

Growth Factors ◽

Growth Factor ◽

Connective Tissue ◽

Endogenous Growth ◽

Cell Lines ◽

Cell Layer ◽

Heparan Sulphate ◽

Myeloid Cells ◽

Myeloid Cell ◽

Gm Csf

In chronic murine schistosomiasis, extramedullar myelopoiesis was observed, with proliferation of myeloid cells in liver parenchyma and in periovular granulomas. We have studied the question of whether cells obtained from granulomatous connective tissue may act as myelopoietic stroma, supporting long-term myeloid proliferation. Primary cell lines (GR) were obtained in vitro from periovular granulomas, induced in mouse livers by Schistosoma mansoni infection. These cells were characterized as myofibroblasts, and represent liver connective tissue cells involved in fibro-granulomatous reactions. They were able to sustain survival and proliferation of the multipotent myeloid cell lines FDC-P1 and DA-1 (dependent on interleukin-3 and/or granulocyte-macrophage colony stimulating factor, GM-CSF) without the addition of exogenous growth factors. This stimulation was dependent upon myeloid cell attachment to the GR cell layer; GR cell-conditioned medium had no activity. Primary murine skin fibroblasts could not sustain myelopoiesis. The endogenous growth-factor was identified as GM-CSF by neutralization assays with monoclonal antibodies. The stimulation of myelopoiesis occurred also when GR cells had been fixed with glutardialdehyde. The observed stimulatory activity was dependent upon heparan sulphate proteoglycans (HSPGs) associated with GR cell membranes. It could be dislodged from the cell layer with heparin or a high salt buffer. Our results indicate a molecular interaction between endogenous growth-factor and HSPGs; this interaction may be responsible for the stabilization and presentation of growth factors in myelopoietic stromas, mediating extramedullar proliferation of myeloid cells in periovular granulomas.

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Retroviral insertions in the murine His-1 locus activate the expression of a novel RNA that lacks an extensive open reading frame

Molecular and Cellular Biology ◽

10.1128/mcb.14.3.1743-1751.1994 ◽

1994 ◽

Vol 14 (3) ◽

pp. 1743-1751

Author(s):

D S Askew ◽

J Li ◽

J N Ihle

Keyword(s):

Cell Lines ◽

Wild Mouse ◽

Myeloid Cell ◽

Single Copy ◽

Open Reading Frame ◽

Chromosome 2 ◽

Coding Region ◽

Reading Frame ◽

Novel Gene ◽

Myeloid Leukemias

The His-1 locus is a common site of viral insertion in murine myeloid leukemias induced by the wild mouse ecotropic retrovirus, CasBrM. In this report, we describe the cloning of a novel gene at the His-1 locus and show that His-1 expression is associated with the transformed phenotype. Northern (RNA) blot analysis identified His-1 transcripts in four transformed myeloid cell lines but in no normal tissues examined. Two of these cell lines were derived from retrovirus-induced myeloid leukemias that harbor integrated proviruses which drive His-1 gene expression by promoter insertion. The two other cell lines expressed a discrete 3-kb His-1 RNA that is derived from a novel gene consisting of three exons that span 6 kb on mouse chromosome 2. The His-1 gene is conserved as a single-copy sequence in multiple vertebrate species and is expressed as a spliced and polyadenylated RNA. A protein-coding region is not evident from analysis of the His-1 sequence because of the presence of multiple small open reading frames, none of which are greater than 219 bp. This lack of an extensive open reading frame is an unusual feature that is shared by other RNA molecules believed to function in the absence of translation.

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Latent Infection and Reactivation of Human Herpesvirus 6 in Two Novel Myeloid Cell Lines

Blood ◽

10.1182/blood.v93.3.991 ◽

1999 ◽

Vol 93 (3) ◽

pp. 991-999 ◽

Cited By ~ 18

Author(s):

Masaki Yasukawa ◽

Hideki Ohminami ◽

Eiji Sada ◽

Yoshihiro Yakushijin ◽

Masahiko Kaneko ◽

...

Keyword(s):

Cell Lines ◽

Philadelphia Chromosome ◽

Human Herpesvirus ◽

Myeloid Cell ◽

Antigen Expression ◽

Cell Lysis ◽

Myelogenous Leukemia ◽

Human Herpesvirus 6 ◽

Latently Infected ◽

Herpesvirus 6

Abstract It has been reported that reactivation of human herpesvirus-6 (HHV-6) causes a failure of hematopoiesis. To clarify the mechanisms of bone marrow suppression induced by HHV-6 infection, it is necessary to establish an in vitro model of HHV-6 infection in hematopoietic progenitor cells. We have established two novel Philadelphia chromosome–positive myeloid cell lines, SAS413 and SAS527, which possess different hematologic characteristics and show distinct susceptibility to infection by HHV-6, from a patient with blast crisis of chronic myelogenous leukemia (CML). HHV-6 subgroup A (HHV-6A) showed marked replication in SAS413, forming syncytia and inducing cell lysis in short-term culture. On the other hand, HHV-6A–inoculated SAS527 continued to proliferate without cell lysis and only a few cells showed HHV-6 antigen expression. In contrast to HHV-6A infection, inoculation with HHV-6 subgroup B (HHV-6B) did not induce any cytopathic effect (CPE) or viral antigen expression in either of the cell lines. Although HHV-6B replication was undetectable, the presence of the HHV-6 genome in both cell lines was shown by polymerase chain reaction (PCR) during culture for more than 10 months, suggesting that HHV-6B latently infected SAS413 and SAS527. Phorbol ester treatment of SAS527 latently infected with HHV-6B resulted in reactivation of HHV-6, as shown by the appearance of a CPE, positive reactivity for the HHV-6 antigen, and isolation of infectious HHV-6. These novel cell lines should be useful for studying the mechanisms of HHV-6–induced hematopoietic failure and HHV-6 latency and reactivation, as well as differentiation, of the myeloid cell lineage.

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