Transforming growth factor‐β1 augments macrophage‐colony stimulating factor activity on human marrow

Rosenfeld, Craig S.

doi:10.1002/stem.5530120509

Cited by 7 publications

(2 citation statements)

References 20 publications

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“…Two early studies have shown induction of c-fms by TGF-h1 in a murine myeloid progenitor cell line and in vascular smooth muscle cells (17,18). In addition, a previous study has suggested that TGF-h1 augments CSF-1 activity in bone marrow (37). Our data show that TGF-h1 induces the mRNA expression of Figure 5.…”

Section: Discussionsupporting

confidence: 76%

Elevated Expression of the Oncogene c-fms and Its Ligand, the Macrophage Colony-Stimulating Factor-1, in Cervical Cancer and the Role of Transforming Growth Factor-β1 in Inducing c-fms Expression

et al. 2007

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Cervical cancer is the third most common gynecologic cancer in the United States. The presence and possible involvement of several cytokines have been studied in cervical cancer; however, very little data, if any, are available on whether cervical tumors are responsive to stimulation by the macrophage colony-stimulating factor-1 (CSF-1). Given the involvement of c-fms and its ligand CSF-1 in gynecologic cancers, such as that of the uterus and the ovaries, we have examined the expression of c-fms and CSF-1 in cervical tumor (n = 17) and normal cervix (n = 8) samples. The data show that c-fms and its ligand are significantly higher in cervical carcinomas compared with normal samples. Immunohistochemistry not only showed that tumor cells expressed significantly higher levels of c-fms but also c-fms levels were markedly higher in tumor cells than tumor-associated stromal cells. Blocking c-fms activity in cervical cancer cells, which express CSF-1 and c-fms, resulted in increased apoptosis and decreased motility compared with control, suggesting that CSF-1/c-fms signaling may be involved in enhanced survival and possibly invasion by cervical cancer cells via an autocrine mechanism. Combined, the data show for the first time the induction of CSF-1 and c-fms in cervical carcinomas and suggest that c-fms activation may play a role in cervical carcinogenesis. Additionally, our data suggest that transforming growth factor-B1 may be a factor in inducing the expression of c-fms in cervical cancer cells. The data suggest that c-fms may be a valuable therapeutic target in cervical cancer. [Cancer Res 2007;67(5):1918-26]

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Section: Discussionsupporting

confidence: 76%

Elevated Expression of the Oncogene c-fms and Its Ligand, the Macrophage Colony-Stimulating Factor-1, in Cervical Cancer and the Role of Transforming Growth Factor-β1 in Inducing c-fms Expression

et al. 2007

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“…Previous studies focusing on TGF-␤1 have shown that this isoform increases or reduces the mitogenic effect of CSF-1 depending on the species, the tissue of origin, and the stage of differentiation of cells from the macrophage lineage (Ohta et al, 1987;C elada and Maki, 1992;Suzumura et al, 1993;Rosenfeld, 1994). Here we found that rhTGF-␤1-␤3 on their own do not support survival of rat BMs or BMMs but markedly enhance the CSF-1-induced proliferation of these phagocytes.…”

Section: Discussionmentioning

confidence: 99%

Neurons Promote Macrophage Proliferation by Producing Transforming Growth Factor-β2

et al. 1997

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The infiltration of bone marrow-derived macrophages into the CNS contributes to growth and reactions of microglia during development or after brain injury. The proliferation of microglial cells is stimulated by colony-stimulating factor 1 (CSF-1), an astrocyte-produced growth factor that acts on mononuclear phagocytes. In the present study, we have shown, using an in vitro model system, that rodent neurons obtained from the developing cerebral cortex produce a soluble factor that strongly enhances the proliferation of macrophages cultured in the presence of CSF-1. Both macrophages isolated from the developing brain and those from the adult bone marrow were stimulated. Kinetic analyses of [ 3 H]thymidine incorporation into macrophages indicated that their response to the neuronderived factor involved a shortening of the cycle of proliferating cells. The effect of neurons on macrophages was blocked in the presence of antibodies neutralizing transforming growth factor-␤2 (TGF-␤2), whereas recombinant TGF-␤2 stimulated macrophage proliferation in the presence of CSF-1. Neuronal secretion of TGF-␤2 was confirmed by reverse transcription-PCR detection of TGF-␤2 transcripts and immunodetection of the protein within neurons and in their culture medium. In situ hybridization and immunohistochemical experiments showed neuronal expression of TGF-␤2 in sections of cerebral cortex obtained from 6-d-old rats, an age at which extensive developmental recruitment of macrophages occurs in this cerebral region. Altogether, our results provide direct evidence that neurons have the capacity to promote brain macrophage proliferation and demonstrate the role of TGF-␤2 in this neuronal function.

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Systemic transforming growth factor-beta in patients with bone marrow fibrosis—pathophysiological implications

et al. 1998

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Idiopathic myelofibrosis (IMF) and secondary myelofibrosis (MF) are characterized by bone marrow (BM) fibrosis, neoangiogenesis, and increased extracellular matrix (ECM) proteins. These characteristics may be partially attributed to transforming growth factor beta (TGF-), a cytokine produced by monocytes. In myelofibrosis, monocytes are increased and activated with concomitant up-regulation of intracytoplasmic TGF-. We have therefore determined systemic TGF-in patients with either BM fibrosis: IMF, n = 18; MF, n = 16; or without BM fibrosis: hematologic disorders with normal platelets (n = 31); high platelets (n = 9); or normal controls (n = 27). Compared with nonfibrosis sera, there was significant TGF-elevation in BM fibrosis sera (P < 0.0001). Most (>80%) of the TGF-is active and belongs to the −1 isoform. In situ hybridization and immunohistochemical analyses in BM biopsy sections showed a marked increase in TGF-1 only in patients with fibrosis. Moreover, TGF-protein was detected mainly in myelomonocytic-like predominant areas. To determine if another functionally similar cytokine, basic fibroblast growth factor (bFGF), may be important to BM fibrosis, we quantitated sera levels and found elevation in 57% compared with 100% elevation for TGF-. The data indicate that irrespective of etiology, systemic TGF-is elevated in patients with BM fibrosis. TGF-likely plays an important role in the development of BM fibrosis. The study also provides a significant parameter for early therapeutic intervention in BM fibrosis. Am.

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Transforming growth factor‐β1 augments macrophage‐colony stimulating factor activity on human marrow

Cited by 7 publications

References 20 publications

Elevated Expression of the Oncogene c-fms and Its Ligand, the Macrophage Colony-Stimulating Factor-1, in Cervical Cancer and the Role of Transforming Growth Factor-β1 in Inducing c-fms Expression

Elevated Expression of the Oncogene c-fms and Its Ligand, the Macrophage Colony-Stimulating Factor-1, in Cervical Cancer and the Role of Transforming Growth Factor-β1 in Inducing c-fms Expression

Neurons Promote Macrophage Proliferation by Producing Transforming Growth Factor-β2

Systemic transforming growth factor-beta in patients with bone marrow fibrosis—pathophysiological implications

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