Synergistic suppression: anomalous inhibition of the proliferation of factor-dependent hemopoietic cells by combination of two colony-stimulating factors.

Metcalf, Donald; Nicola, Nicos A.; Gough, Nicholas M.; Elliott, Michael J.; McArthur, Grant A.; Li, M

doi:10.1073/pnas.89.7.2819

Cited by 15 publications

(6 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consistent with this notion, M-CSF receptor (M-CSFR, also called Fms), a member of the tyrosine kinase receptor family, is prominently expressed on monocytic cells and their progenitors (12,36). Numerous in vitro studies have supported the key role of M-CSF in macrophage production (6,7,38,(41)(42)(43)51). M-CSF was initially defined as the growth factor stimulating production of macrophage colonies from bone marrow cells (51).…”

mentioning

confidence: 99%

Induced Expression and Association of the Mona/Gads Adapter and Gab3 Scaffolding Protein during Monocyte/Macrophage Differentiation

Bourgin

Bourette

Arnaud

et al. 2002

Molecular and Cellular Biology

View full text Add to dashboard Cite

Mona/Gads is a Grb2-related, Src homology 3 (SH3) and SH2 domain-containing adapter protein whose expression is restricted to cells of hematopoietic lineage (i.e., monocytes and T lymphocytes). During monocyte/ macrophage differentiation, Mona is induced and interacts with the macrophage colony-stimulating factor receptor, M-CSFR (also called Fms), suggesting that Mona could be involved in developmental signaling downstream of the M-CSFR by recruiting additional signaling proteins to the activated receptor. Our present results identify Mona as a specific partner protein for the DOS/Gab family member Gab3 in monocytic/ macrophage development. Mona does not interact with Gab2; however, Gab3 also forms a complex with the Mona-related adapter Grb2. Glutathione S-transferase pull-down experiments demonstrate that the Mona and Gab3 interaction utilizes the carboxy-terminal SH3 domain of Mona and the atypical proline-rich domain of Gab3. Mona is known to interact with the phosphorylated Y697 site of the M-CSFR. The M-CSFR mutation Y697F exhibited qualitative and quantitative abnormalities in receptor and Gab3 tyrosine phosphorylation, and Mona induction was greatly reduced. The Y807F M-CSFR mutation is defective in differentiation signaling, but not growth signaling, and also fails to induce Mona protein expression. During M-CSF-stimulated macrophage differentiation of mouse bone marrow cells, Mona and Gab3 expression is coinduced, these proteins interact, and Mona engages in multimolecular complexes. These data suggest that association of Mona and Gab3 plays a specific role in mediating the M-CSFR differentiation signal.

show abstract

mentioning

confidence: 99%

Induced Expression and Association of the Mona/Gads Adapter and Gab3 Scaffolding Protein during Monocyte/Macrophage Differentiation

Bourgin

Bourette

Arnaud

et al. 2002

Molecular and Cellular Biology

View full text Add to dashboard Cite

show abstract

“…4). In contrast, the stromal cells did not express Mac‐1 (Metcalf et al, 1992), c‐fms, F4/80 (Bock et al, 1991), PECAM‐1, and LFA‐1 (Ling et al, 1997) (Fig. 4).…”

Section: Resultsmentioning

confidence: 95%

Detection of murine adult bone marrow stroma‐initiating cells in Lin⁻c‐fms⁺c‐kit^lowVCAM‐1⁺ cells

Tanaka-Douzono

Suzu

Yamada

et al. 2001

Journal Cellular Physiology

View full text Add to dashboard Cite

We attempted to characterize the phenotype of cells which initiate fibroblastic stromal cell formation (stroma-initiating cells: SICs), precursor cells for fibroblastic stromal cells, based on the expression of cell surface antigens. First, we stained adult murine bone marrow cells with several monoclonal antibodies and separated them by magnetic cell sorting. SICs were abundant in the c-kit(+), Sca-1(+), CD34(+), VCAM-1(+), c-fms(+), and Mac-1(-) populations. SICs were recovered in the lineage-negative (Lin(-)) cells but not the Lin(+) cells. When macrophage colony-stimulating factor (M-CSF) was absent from the culture medium, no stromal colony appeared among the populations enriched in SICs. Based on these findings, the cells negative for lineage markers and positive for c-fms (M-CSF receptor) were further divided on the basis of the expression of c-kit, VCAM-1, Sca-1 or CD34 with a fluorescence-activated cell sorter. SICs were found to be enriched in the Lin(-)c-fms(+)c-kit(low) cells and Lin(-)c-fms(+)VCAM-1(+) cells but not in Lin(-)c-fms(+)Sca-1(+) cells and Lin(-)c-fms(+)CD34(low) cells. As a result, the SICs were found to be present at highest frequency in Lin(-)c-fms(+)c-kit(low)VCAM-1(+) cells: a mean of 64% of the SICs in the Lin(-) cells were recovered in the population. In morphology and several characteristics, the stromal cells derived from Lin(-)c-fms(+)c-kit(low)VCAM-1(+) cells resembled fibroblastic cells. The number of Lin(-)c-fms(+)c-kit(low)VCAM-1(+) cells in bone marrow of mice injected with M-CSF was higher than that in control mice. In this study, we identified SICs as Lin(-)c-fms(+)c-kit(low)VCAM-1(+) cells and demonstrated that M-CSF had the ability to increase the cell population in vivo.

show abstract

“…Synergistic suppression either by growth stimulatory cytokines or growth inhibitory cytokines could also lead to the effects observed. 27,28 These experiments provide more insight into our previous study showing that acute myeloid leukemia (AML) blast cells, derived from patients, preincubated with 250 nM bryo-1 commonly showed an increased plating efficiency. Because TNF␣ is known to enhance leukemia cell growth, 29,30 bryo-1-induced TNF␣ release from accessory cells might explain bryo-1-induced spurring of leukemia cell growth.…”

Section: Discussionmentioning

confidence: 97%

Role of TNFα in bryostatin-induced inhibition of human hematopoiesis

et al. 1999

View full text Add to dashboard Cite

In previous studies bryostatin has been shown to cause dosedependent stimulatory or inhibitory effects on colony formation in acute myeloid leukemias. In this study we investigated the inhibitory effect of high dose bryostatin-1 (bryo-1) on normal human bone marrow mononuclear cells (BMNC) colonyforming capacity. Preculturing BMNC for 24 h with 250 nM bryo-1 reduced colony formation by 66 ± 11% whereas this treatment did not reduce clonogenic capacity of highly purified CD34

show abstract

Synergistic suppression: anomalous inhibition of the proliferation of factor-dependent hemopoietic cells by combination of two colony-stimulating factors.

Cited by 15 publications

References 15 publications

Induced Expression and Association of the Mona/Gads Adapter and Gab3 Scaffolding Protein during Monocyte/Macrophage Differentiation

Induced Expression and Association of the Mona/Gads Adapter and Gab3 Scaffolding Protein during Monocyte/Macrophage Differentiation

Detection of murine adult bone marrow stroma‐initiating cells in Lin⁻c‐fms⁺c‐kit^lowVCAM‐1⁺ cells

Role of TNFα in bryostatin-induced inhibition of human hematopoiesis

Contact Info

Product

Resources

About

Synergistic suppression: anomalous inhibition of the proliferation of factor-dependent hemopoietic cells by combination of two colony-stimulating factors.

Cited by 15 publications

References 15 publications

Induced Expression and Association of the Mona/Gads Adapter and Gab3 Scaffolding Protein during Monocyte/Macrophage Differentiation

Induced Expression and Association of the Mona/Gads Adapter and Gab3 Scaffolding Protein during Monocyte/Macrophage Differentiation

Detection of murine adult bone marrow stroma‐initiating cells in Lin−c‐fms+c‐kitlowVCAM‐1+ cells

Role of TNFα in bryostatin-induced inhibition of human hematopoiesis

Contact Info

Product

Resources

About

Detection of murine adult bone marrow stroma‐initiating cells in Lin⁻c‐fms⁺c‐kit^lowVCAM‐1⁺ cells